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My Medicine Notes

It is recommended that all children and adolescents with a new diagnosis of hypertension undergo renal ultrasound and laboratory evaluation for renal pathology (strength of recommendation [SOR]: C, consensus-based guidelines). 

Specific diagnostic tests are recommended for newly diagnosed patients who have suspicious clinical findings suggestive of a secondary cause of hypertension based on the initial history (excess daytime sleepiness, palpitations, tremor, sweating); physical examination (abdominal bruit, thyromegaly, malar rash); or laboratory analysis (elevated serum creatinine, low thyroid-stimulating hormone) (SOR: C, consensus-based guidelines). 

Patients with undifferentiated resistant hypertension should receive further directed evaluation for secondary causes (SOR: C, consensus-based guidelines).


Children:

Secondary hypertension is more prevalent in younger children and in children and adolescents with stage 2 hypertension (blood pressure [BP] >99th percentile for age and height plus 5 mm Hg).1 Renoparenchymal and renovascular disease account for most cases of secondary hypertension in these children.

70% to 85% of children <12 years and 10% to 15% of adolescents 12 to 18 years with hypertension have an underlying cause, most commonly renoparenchymal and renovascular disease.

Such evaluation should include a renal ultrasound and laboratory testing (creatinine, urinalysis, and urine culture) to look for structural or functional anomalies.

Adults:

Secondary hypertension reportedly occurs in 5% to 10% of hypertensive patients.

Patients at highest risk for secondary hypertension have no family history of hypertension; abrupt onset, symptomatic, or crisis hypertension; stage 2 hypertension; sudden loss of hypertensive control; and drug-resistant hypertension.

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recommends that patients with the following characteristics undergo further directed evaluation for a secondary cause:8

  • younger than 30 years with no family history of hypertension
  • older than 55 years with new hypertension
  • abdominal bruit with diastolic component
  • sudden worsening of BP control
  • recurrent flash pulmonary edema
  • renal failure with abnormal urinary sediment or proteinuria
  • acute renal failure after administration of an ACE inhibitor or ARB.

Patients with resistant hypertension (BP>140/90 mm Hg despite taking optimal doses of 3 antihypertensive medications, one of which is a diuretic) should receive particular scrutiny for an identifiable secondary cause.

References:

  • J Fam Pract. 2014 January;63(1):41-42,54.
Источник: https://rensbox.duckdns.org/medsmart.html

Gender and Dermatology by Ethel Tur, Howard I. Maibach (Eds.) PDF

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Dermatology

Ethel Tur
Howard I. Maibach
Editors

123
Gender and Dermatology
Ethel Tur  •  Howard I. Maibach
Editors

Gender and Dermatology


Editors
Ethel Tur Howard I. Maibach
Tel Aviv University Department of Dermatology
Tel Aviv UCSF Medical Center
Israel San Francisco
CA
USA

ISBN 978-3-319-72155-2    ISBN 978-3-319-72156-9 (eBook)


https://doi.org/10.1007/978-3-319-72156-9

Library of Congress Control Number: 2018936629

© Springer International Publishing AG, part of Springer Nature 2018


This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or
part of the material is concerned, specifically the rights of translation, reprinting, reuse of
illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way,
and transmission or information storage and retrieval, electronic adaptation, computer software,
or by similar or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this
publication does not imply, even in the absence of a specific statement, that such names are
exempt from the relevant protective laws and regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in
this book are believed to be true and accurate at the date of publication. Neither the publisher nor
the authors or the editors give a warranty, express or implied, with respect to the material
contained herein or for any errors or omissions that may have been made. The publisher remains
neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Printed on acid-free paper

This Springer imprint is published by the registered company Springer International Publishing
AG part of Springer Nature
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Preface

The nature of certain diseases is different between women and men. Genetic
and hormonal differences affect skin structure and function, thus affecting
disease processes. In addition, exogenous factors differ according to differ-
ences in lifestyle between the sexes. In the last two decades it has been recog-
nized that women are more different medically than previously appreciated,
and studies started being conducted accordingly. Methodologies used in der-
matological research have improved substantially, providing means of objec-
tive evaluation of skin function and characteristics, leading to improvement
in treatment and disease outcome.
Diseases differ between men and women in terms of prevention, clinical
signs, therapeutic approach, prognosis, and psychological and social impacts.
This book outlines several aspects of differences between the skin of
women and men in health and disease, based on available data. It is not
designed to be exhaustive in its coverage of the subject, but rather to highlight
certain aspects of it. We wish and hope that this book will ignite more interest
in the topic of gender dermatology.
The editors are grateful to all our contributing authors for their efforts and
cooperation in applying their knowledge and skill.
Special thanks to our team at Springer: Mr. Grant Weston, Responsible
Editor, Mr. Andre Tournois, Project Coordinator, Mr. Karthik Periyasamy,
Production editor, and Mr. Dinesh Vinayagam, Project Manager, for their
meticulous work.

Tel Aviv, Israel Ethel Tur


San Francisco, CA, USA Howard I. Maibach

v
Contents

1 Effects of Gender on Skin Physiology


and Biophysical Properties. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Richard Randall Wickett and Greg G. Hillebrand
2 Racial and Gender Influences on Skin Disease . . . . . . . . . . . . . 11
Daniel Callaghan and Neelam A. Vashi
3 Aging of the Skin. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25
Enzo Berardesca, Norma Cameli, and Maria Mariano
4 Hair and Scalp Variation Related to Gender. . . . . . . . . . . . . . . 31
Ferial Fanian and Alexandre Guichard
5 Nail Variations Related to Gender . . . . . . . . . . . . . . . . . . . . . . . 43
Robert Baran and Doug Schoon
6 Cutaneous Autoimmune Connective Tissue Disorders. . . . . . . 53
Wohl Yonit
7 Gender Differences in Psoriasis. . . . . . . . . . . . . . . . . . . . . . . . . . 63
Sivan Sheffer Levi and Yuval Ramot
8 Gender Dermatology: Pigmentation Disorders. . . . . . . . . . . . . 83
Mor Pavlovsky
9 Gender and Genodermatoses. . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
Sivan Sheffer Levi and Vered Molho-Pessach
10 Specific Dermatoses of Pregnancy. . . . . . . . . . . . . . . . . . . . . . . . 127
Arieh Ingber
11 Nipples: A Sensitive Topic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139
Eve Finkelstein, Deena Yael Meerkin, and Gina Weissman
12 Acne Vulgaris. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   171
Gila Isman Nelkenbaum
13 Melanocytic Nevi: Patterns and Gender Differences. . . . . . . . . 181
Miryam Kerner
14 Clinical and Therapeutic Considerations of Acquired
Melanocytic Nevi. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 189
Baruch Kaplan

vii
viii Contents

15 Biology and Sex Disparities in Melanoma Outcomes . . . . . . . . 193


Adi Nosrati and Maria L. Wei
16 Infantile Hemangioma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215
Shoshana Greenberger
17 Cutaneous Leishmaniasis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 227
Michal Solomon and Eli Schwartz
18 Fungal Infections (Onychomycosis, Tinea Pedis,
Tinea Cruris, Tinea Capitis, Tinea Manuum,
Tinea Corporis, different Candida Infections,
and Pityriasis Versicolor) and Mycological
Laboratory Analyses. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235
Avner Shemer and Meir Babaev
19 Atopic Dermatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 243
Vered Atar-Snir
20 Occupational Dermatitis in Nail Salon Workers. . . . . . . . . . . . 249
Liran Horev
21 Universal Concepts of Beauty and Their Implications
on Clinical Approach to Female Cosmetic Patient . . . . . . . . . . 255
Marina Landau
22 Gender Differences in Mohs Micrographic Surgery. . . . . . . . . 267
Yoav C. Metzger
23 Gender Differences in Facial Rejuvenation. . . . . . . . . . . . . . . . 271
Benjamin C. Garden and Jerome M. Garden
24 The Skin as a Metaphor: Psychoanalytic
and Cultural Investigations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
Shlomit Yadlin-Gadot and Uri Hadar
Index. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .   299
Effects of Gender on Skin
Physiology and Biophysical 1
Properties

Richard Randall Wickett and Greg G. Hillebrand

Abbreviations corneum (SC) hydration measured by electrical


properties, skin viscoelasticity and facial skin
N.S. No significant difference wrinkling.
SC Stratum corneum
TEWL Transepidermal water loss
1.2 Sebum Production

On average sebum production is approximately


1.1 Introduction the same between men and women up to about
age 50. However, there is extreme variability
This chapter will review the literature on gender between individuals. Pochi et al. measured sebum
differences in skin physiology focusing on non-­ production rates in men and women between the
invasive biophysical measures of skin function. ages of 40 and 79 over a three-hour period using
While there are countless studies on the biophys- absorbent paper on the forehead [1]. Results are
ical properties of human skin, there are fewer presented in Table 1.1.
that examine gender differences. Many studies Sebum production clearly drops off in women
are sponsored by the cosmetic industry and not after age 50 probably because of menopause. In
surprisingly focus on women and often compare all age groups, even 70–79, there was consider-
effects of aging or photoaging. Unfortunately, able overlap between the ranges measured with
the literature that explores gender differences higher sebum producing women producing more
does not always present a clear picture as will be sebum in 3 h than lower producing men.
seen. This contribution will review sebum pro- A more comprehensive study of gender differ-
duction, skin pH, barrier function as assessed by ences in skin sebum production is that by
transepidermal water loss (TEWL), stratum Luebberding et al. [2]. The authors investigated
300 women and men between the ages of 20 and
74. Sebum production was measured on the
R. R. Wickett (*)
James L. Winkle College of Pharmacy, cheeks and foreheads using the Sebumeter [3].
University of Cincinnati, Cincinnati, OH, USA Mean values and standard deviations and statisti-
e-mail: wicketrr@ucmail.uc.edu cal significance levels (p values) for each age
G. G. Hillebrand range and over the entire age range are given in
Global Discovery, Research and Development, Table 1.2. There were 30 subjects of each sex in
Amway Corporation, Ada, MI, USA each age range.
e-mail: greg.hillebrand@Amway.com

© Springer International Publishing AG, part of Springer Nature 2018 1


E. Tur, H. I. Maibach (eds.), Gender and Dermatology,
https://doi.org/10.1007/978-3-319-72156-9_1
2 R. R. Wickett and G. G. Hillebrand

Table 1.1  Sebum production rates and ranges in female and male subjects
Age range Number F/M Femalea Rangea Malea Rangea
40–49 31/50 1.86 0.12–4.80 2.39 0.54–5.14
50–59 21/14 1.08 0.07–2.38 2.43 1.05–4.36
60–69 18/14 0.88 0.22–1.62 2.42 0.83–4.95
70–79 12/13 0.85 0.33–2.19 1.69 0.63–3.23
Sebum production in mg/10 cm2 of skin in 3 h data from Pochi et al. [1]
a

Table 1.2  Sebum levels on the forehead for females and trode at the skin surface with a hydrated skin-­
males
electrode interface [5]. In healthy skin, surface
Age range Femalea SD Malea SD p pH is lower than physiological pH ranging from
20–29 115.50 57.13 120.77 50.24 NS about 4.5–5.5 on most body sites under most con-
30–39 114.82 63.60 127.53 53.87 NS ditions. There has been increasing interest in the
40–49 130.77 63.74 125.93 50.27 NS
role of skin surface pH in maintaining a healthy
50–59 96.73 61.25 125.93 59.66 <0.05
stratum corneum barrier [5].
60–74 66.89 43.68 139.10 66.84 <0.001
Measurements of gender differences in skin
20–74 105.45 61.66 105.45 61.66 <0.001
pH have not produced completely consistent
a
Sebum measurement in μg/cm2 data from Luebberding
et al. [2]
results though there is a trend for females to have
slightly higher pH than males. Table 1.3 shows a
summary of results from several labs comparing
While the overall mean was smaller for the skin surface pH in men vs. women at various
women than men, significant differences were body sites and age groups. Table 1.3 doesn’t pres-
not seen before the 50–59 age group in agree- ent specific pH values because in some cases the
ment with the results of Pochi et al. above. Note authors only provide graphical data so exact
the large standard deviations indicating the large numerical values are not available. Luebberding
variation in sebum production across the sample et al. present numerical pH data and found that
populations. Sebum production on the cheek was males have significantly lower pH on every body
lower than on the forehead but age and sex differ- site for every age group [2]. The overall averages
ences showed very similar trends. Firooz et al. were 5.12 for females and 4.58 for males. This
[4] also reported lower sebum production in was among the largest differences seen in any of
females compared to males in pooled data from the papers reviewed. Zlotogorski [6] found 5.1
several age groups and body sites. Among all on the cheek for males and 5.2 on the cheek for
the skin parameters reviewed in this work, females and the difference was not statistically
lower sebum production in females compared significant. In contrast Ehlers and Ivens [7]
to males above the age of 50 was observed most reported higher skin pH in males (5.8) compared
consistently. to females (5.5) on the forearm.
In a large cross-sectional study of skin condi-
tion, Hillebrand and colleagues measured cheek
1.3 Skin Surface pH and forearm skin surface pH in 450 subjects (191
males, 259 females) ranging in age for 9–78. The
pH is defined as ‘the negative logarithm of the subjects were art festival goers (ArtPrize 2015,
hydrogen ion concentration’. The most common Grand Rapids Michigan) who happened to walk
method for measuring the skin’s surface pH is to by the study venue and volunteered to be partici-
apply a flat surface membrane electrode hydrated pants. Thus, subjects were literally recruited off
with distilled water to the skin surface and mea- the street and represent a real world sampling of
sure the apparent pH. This leads to the definition the local population. Furthermore, the skin was
of skin surface pH in bioengineering terms as: not washed or prepared in any manner prior to
‘apparent pH as measured by a flat glass elec- making the measurement in order to measure an
1  Effects of Gender on Skin Physiology and Biophysical Properties 3

Table 1.3  Skin pH results from various authors


Age range Number F/M Body site Result Reference
20–60 292/282 Forehead M = F Zlotogorski [6]
20–60 292/282 Cheek M = F Zlotogorski [6]
21–37 37/46 Face M < F Kim [8]
13–70 354/304 Forehead M < F Man [9]
0–12 142/128 Forearm M < F Man [9]
36–50 82/60 Forearm M < F Man [9]
51–70 28/31 Forearm M < F Man [9]
70+ 31/24 Forearm M = F Man [9]
70+ 31/24 Forehead M = F Man [9]
20–74 150/150 Forehead M < F Luebberding [2]
20–74 150/150 Cheek M < F Luebberding [2]
20–74 150/150 Neck M < F Luebberding [2]
20–74 150/150 Forearm M < F Luebberding [2]
20–74 150/150 Hand M < F Luebberding [2]
Not reported 6/6 Forearm M > F Ehlers [7]
9–78 259/191 Forearm M < F Hillebranda
9–78 259/191 Cheek M = F Hillebranda
a
G. G. Hillebrand unpublished data

unadulterated apparent pH. Skin pH ranged as have investigated possible gender differences


low as pH 3.1 to as high as pH 6.8 or nearly 4 in TEWL with varying results. Some of the
orders of magnitude in hydronium ion concen- results are presented in Table 1.4. Luebberding
tration! While there was no significant gender- et al. [2] reported higher TEWL in males than
dependent difference in cheek skin pH in females with significant differences on the
(mean ± SD: 5.28 ± 0.43 for males and forehead, cheek, neck and forearm. Chilcott
5.23 ± 0.47 for females), males showed signifi- and Farrar [12] reported higher TEWL in
cantly (p < 0.001) lower forearm skin pH com- males compared to females on the forearm and
pared to females (mean ± SD: 4.59 ± 0.61 for Firooz et al. [4] also reported higher TEWL in
males vs. 4.78 ± 0.65 for females). Figure 1.1 males in pooled data from eight body sites.
shows the percentage of males and females in Wilhelm et al. [13] and Hadi et al. [14] did not
specific pH ranges from pH 3 to pH 7. Females observe any significant effect of gender on
tend to skew to higher pH in accord with the dif- TEWL.
ference in the population means. What is note- Chilcott and Farrar [12] used the ServoMed
worthy is the large overlap in the wide bell EP-2 Evaporimeter (ServoMed, Kinna,
curves for skin pH frequencies between males Sweden) to measure TEWL while Luebberding
and females. Thus, the difference in mean pH et al. [2] used the TEWAmeter® TM300
between genders is small compared to the vari- (Courage & Khazaka, Cologne, Germany).
ance for the entire population (Hillebrand, This may in part explain the higher forearm
unpublished data). results seen by Luebberding. While results
from the two instruments correlate very well,
TEWAmeter data tend to be up to two times
1.4 Transepidermal Water Loss higher than ServoMed data [11, 15]. Li et al.
[16] also reported lower TEWL in female sub-
Measurement of TEWL [10] has been shown jects compared to males in Chinese subjects
to be a valid method to evaluate skin barrier from two age groups, 18–25 and 40–50 on vari-
function in-vivo [11]. Several researchers ous body sites.
4 R. R. Wickett and G. G. Hillebrand

Fig. 1.1  Percent of 40


subjects (frequency %)
having forearm pH Males (n=191)
values in a specific pH Females (n=259)
range
30

Frequency % 20

10

0
0

.5

.0
0

7.
4.

4.

5.

6.

6.
.0

3.

>7
<3

6-

1-

6-

6-

1-

6-
0-

6.
3.

4.

4.

5.

6.
3.

Forearm pH Range

Table 1.4  TEWL females and males


Ages No. (F/M) Body site Female Male P Reference
20–74 150/150 Forehead 10.51 9.29 P < 0.01 Luebberding [2]
20–74 150/150 Cheek 11.15 10.34 P < 0.05 Luebberding [2]
20–74 150/150 Neck 9.25 6.96 P < 0.001 Luebberding [2]
20–74 150/150 Forearm 9.10 5.50 P < 0.001 Luebberding [2]
20–74 150/150 Hand 11.52 10.92 N.S. Luebberding [2]
18–28 10/8 Forearm 4.68 4.98 P < 0.05 Chilcott [12]
10–60 25/25 8 sites 9.52 15.49 P < 0.05 Firoz [4]
N.S. no significant difference

1.5 Stratum Corneum Hydration Table 1.5  Capacitance by body site and gendera
Body site Female Male P value
The stratum corneum needs to maintain proper Forehead 52.94 50.94 N.S.
hydration in order to function properly and lack of Cheek 60.81 57.62 P < 0.05
adequate moisture in the SC can lead to dry skin. Neck 54.34 59.62 P < 0.001
Instrumental methods to measure SC hydration Forearm 44.07 43.10 N.S.
in-vivo rely on measuring either surface conduc- Hand 38.62 32.49 P < 0.001
tance or capacitance [17–20]. Luebberding et al. a
Data from Luebberding et al. [2]. 150 subjects of each
[2] measured skin hydration with the CM 825® sex in each age group. Age range = 20–74. N.S. no signifi-
cant difference
(Courage & Khazaka, Cologne Germany) on five
body sites on 150 subjects of each gender broken
into five age groups. Results from each body site, were not statistically significant. Li et al. [16] found
pooled by age are presented in Table 1.5. females to haves significantly higher hydration on
Females showed higher hydration on the cheek the décolletage are but no other body sites. Neither
and hand while males had higher values on the Firooz et al. [4] nor Wilhelm et al. [13] reported
neck. Differences on the forehead and forearm significant gender differences in hydration.
1  Effects of Gender on Skin Physiology and Biophysical Properties 5

1.6 Elasticity MPA 580 to measure skin elasticity in 25 females


and 25 males ages 10–60. While women had
Skin is a viscoelastic material. It has the unique slightly higher elasticity than men, the difference
ability to rebound after being stretched allowing was not statistically significant. More recently,
itself to return to its initial size and maintain a Hadi et al. [14] used the DermaLab® Combo to
tight covering over the body surface. measure the skin elasticity on the forearm of 50
Unfortunately, skin elasticity declines after the males and 50 females, ages 18–27. Females
third decade in both men and women, especially showed slightly higher skin elasticity than males
on chronically sun-exposed skin sites [21–23]. but the difference was not statistically significant.
This loss in elasticity is likely the major driver for Finally, Ma et al. [32] used the Cutometer MPA
visible facial skin wrinkling and sagging [24]. 580 to measure skin elasticity on the forehead
Skin elasticity is commonly measured using the and cheek of 240 healthy male and female volun-
non-invasive suction method [25–27]. The teers living in Shanghai, aged 20–70 years. There
Cutometer® is one of the more widely used was no significant difference in forehead skin
suction-­based skin elasticity instruments because elasticity between the genders. However, the
of its portability, speed and simplicity researchers did observe lower cheek skin elastic-
(Courage + Khazaka Electronic, Koln, Germany). ity (both R5 and R7) in older (age 50–70) males
The stress/strain curve can be divided into differ- than females. In summary, while skin elasticity
ent regions such as maximum deformation (Uf) declines with age in both males and females,
and immediate retraction (Ur). Ratios of these gender-­associated differences in skin elasticity at
absolute parameters yield relative parameters of any given age are small and likely not clinically
skin elasticity (e.g. Ur/Uf or R7) that are inde- meaningful.
pendent of skin thickness. Nedelec et al. [28]
used the Cutometer MPA 580 with a 6-mm probe
to measure skin elasticity at 16 body sites on 121 1.7 Facial Wrinkling
males and 120 females who were mostly Asian or
Caucasian and aged between 20 and 85 years old. When it comes to facial wrinkling, which sex
They found no consistent trend for gender differ- ages faster, men or women? Chung et al. [33]
ences in skin elasticity (R7) across age groups. assessed facial wrinkling on 236 men and 171
Cua et al. [29] also did not observe a significant women using standardized visual grading scales.
difference in skin elasticity between males and The results suggest that while the pattern of facial
females though their sample size was very small. wrinkling is similar between the sexes, women
Ishikawa et al. [30] compared skin elasticity on showed more severe wrinkles after adjusting for
men vs. women in a large subject sample on mul- age, sun exposure and smoking. Gender-­
tiple skin sites. Specifically, they used the dependent differences in facial wrinkling should
Cutometer SEM 474 to measure skin elasticity also consider facial location. In the perioral
on the forearm, hand, finger and chest of 96 males region (upper lip), women exhibit more and
and 95 females ages 9–87. Again, there was no deeper wrinkles than men [34]. However, on the
significant difference in skin elasticity between forehead, men show an earlier onset and more
males and females. Luebberding et al. [31] used severe wrinkling at every age than women [32].
the Cutometer MPA 580 to measure skin elastic- Hamer et al. [35] measured facial wrinkling using
ity on the cheek, neck and dorsum of the hand in digital imaging in 3831 Europeans (58% female)
150 males and 150 females ages 20–74. Skin aged 51–98. Men had higher wrinkle area than
elasticity (Ur/Uf) declined with age in both gen- women in the younger age groups (<75) but
ders, but was only slightly higher in women than women showed more wrinkles in the older age
in men. The authors noted that there was a more group (>75). Chien et al. [36] developed photo-
rapid decline in elasticity in women after 40 years graphic scales for perioral and crow’s feet wrin-
of age. Firooz et al. [4] also used the Cutometer kles that were gender specific meaning that there
6 R. R. Wickett and G. G. Hillebrand

was a scale for men and a scale for women. They sebaceous gland density. Sebaceous gland den-
used the grading scales to assess facial wrinkling sity was found to be significantly lower in the
on 71 men and 72 women, aged 21–91 years. All lateral canthus than in the forehead on both males
subjects were graded using both scales. and females. However, while the sebaceous gland
Interestingly, a participant’s score on the female-­ density was significantly lower in females than in
specific scale differed significantly from the males in both facial regions, there was no signifi-
male-specific scale score showing that it is cant gender-dependent difference in wrinkle
important to use gender-specific scales for the depth.
visual grading of facial wrinkling. The research- In a cross-sectional study of skin condition,
ers found that perioral wrinkling was more severe Hillebrand and colleagues measured facial wrin-
in women than men. For participants older than kling in the periorbital area (under eye and crow’s
45 years, there was even greater gender disparity. feet wrinkles) on 147 Caucasian males and 183
Tsukahara et al. measured facial wrinkling in 173 Caucasian females, aged 10–78. Regression anal-
Japanese men and women [37]. Men showed ysis showed that both gender and age to be sig-
increased forehead wrinkles compared with nificant (p < 0.05) factors in describing the
women at all ages. However, the difference in variance in wrinkle severity (Fig. 1.2a). However,
facial wrinkle severity tended to disappear in the when other factors are considered in the regres-
older age groups and there were no gender-­ sion analysis, like the subject’s body mass index,
related differences at any age for upper eyelid smoking history in pack years and years working
wrinkles. In related work, 3D analysis of skin outside, gender drops out as a significant factor
replicas found that the depth of eye wrinkles in suggesting that some of the variance initially
men showed an annual variation with more wrin- explained by gender can be explained by other
kles at the corner of the eye in the fall compared gender-associated confounding factors. We will
to the spring; no such annual variation was discuss confounding factors more later in the
observed in women [38]. The varying density of chapter. Figure 1.2b shows the data in Fig. 1.2a
sebaceous glands on the face may partly explain replotted as age group means for males and
the variation in facial wrinkling at different facial females. While females had higher wrinkles than
sites. Tamatsu et al. [39] looked at cadaver skin men in all age groups, none of the pairwise com-
specimens from females and males ranging in parisons between males and females in any given
age from the 20s to 90s at age of death. The found age group were significantly different (one-way
a negative correlation between wrinkle depth and ANOVA, Tukey Test).

a 0.16 b 0.08
Females
0.14 Females
Periorbital W rinkle Severity

Males
Periorbital W rinkle Severity

Males
(wrinkle area fraction)

0.12 0.06
(wrinkle area fraction)

Females
(r2=0.63)
0.10

0.08 0.04
0.06
Males
(r2=0.58)
0.04 0.02
0.02

0.00
0.00
0 20 40 60 80 100
10-19 20-29 30-39 40-49 50-59 60-69 70-79
Age Age Range

Fig. 1.2  Wrinkle severity in the periorbital region for sent best fit linear regression curves. (b) Age group
Caucasian females and males. (a) Scatter plot where each means ± standard error
point represents a subject’s wrinkle severity. Lines repre-
1  Effects of Gender on Skin Physiology and Biophysical Properties 7

1.8 Confounding Factors dition and most enroll only females. In a cross-­
sectional study of 4025 women ages 40–74,
The differences observed between male and Cosgrove et al. found that higher intakes of vita-
female skin may be ascribed to intrinsic factors min C and linoleic acid and lower intakes of fats
like hormones [40] and other genetically deter- and carbohydrates are associated with better
mined variables or extrinsic factors like differ- skin-aging appearance [48]. Higher intakes of
ences in smoking, diet, sun protection and skin vegetables, fruit, olive oil, and legumes may
care routines. Even differences in facial expres- cause less skin wrinkling and are protective
sion patterns may differ between the sexes and against actinic damage [49]. Iizaka et al. mea-
influence skin condition, especially facial wrin- sured nutritional status and habitual dietary
kling [41]. Below we discuss confounding fac- intact, stratum corneum hydration and xerosis in
tors that should be considered when designing 118 older (>65) Japanese subjects, mostly
and interpreting clinical data for men and women. females [50]. They concluded that a dietary pat-
tern characterized by higher vegetable and fruit
intake was associated with a better skin condi-
1.8.1 Smoking History tion. Since men’s daily intake of fruits and vege-
tables is less than that of women [51], dietary
Smoking has been shown to increase facial wrin- differences in the sample population should be
kling [34]. A report by Okada et al. involving considered in interpretation and analysis of clini-
identical twins underscores the risk of smoking cal results as well as in clinical design.
on appearance and health. They compared facial
wrinkling in identical twins and showed that a
5-year difference in smoking history can have a 1.8.3 Skin Care Habits and Practices
noticeable effect on skin aging [42]. Similar
observations were reported by Doshi et al. [43]. A person’s daily skin care routine will undoubt-
The exact mechanism for how smoking affects edly affect their skin condition. Regular use of
skin wrinkling is not understood but may involve moisturizers will improve skin barrier function,
changes in skin barrier function and associated skin hydration, and lessen the advancement of
changes in chronic skin dryness caused both by wrinkling [14, 41]. Those who regularly protect
smoking and exposure to second-hand smoke their skin from acute and chronic sun exposure
[44] which is associated with having more wrin- will slow the advancement of skin aging. Male
kles [41, 43, 44]. Since men are more likely to facial skin is largely influenced by beard groom-
smoke than women (Centers for Disease Control ing routines [52, 53]. In this regard, many of the
and Prevention [45], smoking needs to be consid- differences observed between male and female
ered as a confounding variable when comparing skin may be attributable to differences in skin
the skin condition of males to females. care habits and practices, especially differences
on the face [54].

1.8.2 Diet and Nutrition


1.8.4 Sun Exposure
Consuming an adequate amount of fruit and veg-
etables has been shown to reduce the risk of Sun exposure is well known to be a major cause
excess weight gain, type 2 diabetes, cardiovascu- of wrinkling, especially in facial skin [23, 55–
lar disease, and specific cancers [46, 47]. Pezdirc 57]. When discussing gender differences in facial
et al. [47] has recently reviewed the summation wrinkles the relative tendency for sun exposure
of evidence linking diet and skin health. The and the frequency of sunscreen application
majority of studies conducted in this space focus should be considered as regular sunscreen use
on the effect of dietary supplements on skin con- may provide some protection against the signs of
8 R. R. Wickett and G. G. Hillebrand

photoaging [58, 59]. Haluza et al. reported that 3. Ogoshi K. Optical measurement of sebum excre-
tion using opalescent film imprint. The Sebumeter.
Australian men are more likely to suffer sun
In: Handbook of non-invasive methods and the skin.
exposure and less likely to use sunscreen com- Boca Raton: Taylor and Francis; 2006. p. 841–6.
pared to their female counterparts [60]. This may 4. Firooz A, Sadr B, Babakoohi S, Sarraf-Yazdy M,
explain the earlier onset [35] and more severe Fanian F, Kazerouni-Timsar A, et al. Variation of bio-
physical parameters of the skin with age, gender, and
wrinkling seen in men on the forehead [37] but is
body region. Sci World J. 2012;2012:386936.
not consistent with the higher levels of perioral 5. Fluhr JW, Bankova L, Dikstein S. Skin surface pH:
wrinkles seen in women [36]. mechanism, measurement, importance. In: Serup J,
GBE J, Grove GL, editors. Handbook of non-invasive
methods and the skin. 2nd ed. Boco Raton: Taylor and
Francis; 2006. p. 411–20.
1.9 Summary 6. Zlotogorski A. Distribution of skin surface pH on the
forehead and cheek of adults. Arch Dermatol Res.
One of most important and difficult questions 1987;279(6):398–401.
7. Ehlers C, Ivens UI, Møller ML, Senderovitz T, Serup
whenever comparing measured properties
J. Females have lower skin surface pH than men. Skin
between two groups is whether statistically sig- Res Technol. 2001;7(2):90–4.
nificant differences are clinically relevant. We 8. Kim MK, Patel RA, Shinn AH, Choi SY, Byun HJ,
have reviewed and summarized many of the stud- Huh CH, et al. Evaluation of gender difference in skin
type and pH. J Dermatol Sci. 2006;41(2):153–6.
ies aimed at improving our understanding of the
9. Man MQ, Xin SJ, Song SP, Cho SY, Zhang XJ, Tu
similarities and differences between male and CX, et al. Variation of skin surface pH, sebum con-
female skin with particular attention to differ- tent and stratum corneum hydration with age and
ences in biophysical skin properties. We noted gender in a large Chinese population. Skin Pharmacol
Physiol. 2009;22(4):190–9.
that results depended on the method used, the
10. Nilsson GE. Measurement of water exchange through
body site being measured, the age of the subjects, the skin. Med Biol Eng Comput. 1977;15:209–18.
and their prior history of smoking, sun exposure, 11. Fluhr JW, Feingold KR, Elias PM. Transepidermal
and use of skin care products. The most consis- water loss reflects permeability barrier status: valida-
tion in human and rodent in vivo and ex vivo models.
tent difference between the genders reported in
Exp Dermatol. 2006;15(7):483–92.
this review is lower sebum production in women, 12. Chilcott RP, Farrar R. Biophysical measurements of
especially over the age of 50. However, because human forearm skin in vivo: effects of site, gender,
of the high individual variability in sebum output chirality and time. Skin Res Technol. 2000;6(2):64–9.
13. Wilhelm KP, Cua AB, Maibach HI. Skin aging. Effect
there is overlap between the high sebum produc-
on transepidermal water loss, stratum corneum hydra-
ing females and low sebum producing males tion, skin surface pH, and casual sebum content. Arch
(Table 1.1). Thus care must be taken when draw- Dermatol. 1991;127(12):1806–9.
ing conclusions from the differences reported in 14. Hadi H, Awadh AI, Hanif NM, Md Sidik NF, Mohd
Rani MR, Suhaimi MS. The investigation of the skin
the studies summarized here.
biophysical measurements focusing on daily activi-
ties, skin care habits, and gender differences. Skin Res
Acknowledgements The authors wish to thank Aimee Technol. 2016;22(2):247–54.
Herbel (Amway Corporation) for her help in collecting 15. Barel AO, Clarys P. Study of the stratum corneum
the pH data in Fig. 1.1. barrier function by transepidermal water loss mea-
surements: comparison between two commercial
instruments: Evaporimeter and Tewameter. Skin
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Racial and Gender Influences
on Skin Disease 2
Daniel Callaghan and Neelam A. Vashi

2.1 Introduction 2.1.1 Physiologic Differences

Skin of color typically refers to individuals of 2.1.1.1 Skin Physiology


African, Afro-Caribbean, Asian, Hispanic, Skin is routinely characterized by the Fitzpatrick
Native American, Middle Eastern and Pacific scale, a classification scheme based on how one
Island backgrounds. In the United States, indi- reacts to sun exposure. Type I skin is fair, burns
viduals from these groups made up 38% of the easily and does not tan. Type VI skin is dark
population in 2014, which is expected to increase brown or black, tans and never burns. Although
to 56% by 2060 [1]. large variation exists within the SOC population
Due to differences in skin physiology as well (SOC), generally speaking, SOC is generally rep-
as to different cultural practices, there are several resented by Fitzpatrick types III–VI skin.
dermatologic conditions that affect these popula- The hallmark feature of skin of color is the
tions at a higher rate compared to Caucasians. amount and distribution of melanin. Darker skin
Furthermore, there are a number of diseases that phenotypes have larger, non-aggregating melano-
disproportionately affect males and females somes distributed throughout the epidermis.
within these populations. In this chapter, we will Conversely, fairer skinned individuals have
discuss categories of diseases that are more com- smaller, aggregated melanosomes which are not
monly seen in these ethnic groups, including fol- present in the upper layers of the epidermis [2].
licular, scarring, and pigmentary disorders with a Due to this increased melanin, Black skin trans-
special focus on their epidemiology and mits only 7.4% of ultraviolet (UV) radiation,
pathogenesis. compared to 29.4% in Caucasian skin [3]. While
this pigmentation offers protection against some
diseases seen more commonly in Caucasians,
such as non-melanoma skin cancer, it makes those
with darkly pigmented skin more susceptible to
other diseases, particularly pigmentary disorders.
D. Callaghan
Boston University Medical Center, Boston, MA, USA The stratum corneum in skin of color is more
e-mail: daniel.callaghan@bmc.org compact due to greater intercellular cohesion.
N. A. Vashi (*) Although there is no difference in dermal thick-
Dermatology, Boston University Center for Ethnic ness, Black skin has more numerous and larger
Skin, Boston University School of Medicine, fibroblasts, which is thought to partially explain
Boston, MA, USA why they are at an increased risk of keloid
e-mail: nvashi@bu.edu

© Springer International Publishing AG, part of Springer Nature 2018 11


E. Tur, H. I. Maibach (eds.), Gender and Dermatology,
https://doi.org/10.1007/978-3-319-72156-9_2
12 D. Callaghan and N. A. Vashi

f­ ormation. Additionally, Black skin has collagen 2.2  ollicular and Scarring


F
fibers that are smaller but more closely stacked Disorders
together. Of note, studies regarding physiologic
differences in eccrine, apocrine and sebaceous 2.2.1 C
 entral Centrifugal Cicatricial
glands in different races have demonstrated con- Alopecia
flicting results [2, 4].
2.2.1.1 Introduction
2.1.1.2 Hair Physiology Central centrifugal cicatricial alopecia (CCCA),
Individuals of African descent have hair that is formerly known as hot comb alopecia or follicu-
characterized by flat, elliptical strands with lar degeneration syndrome, is a disease seen
curved follicles, which leads to tightly spiraled almost exclusively in African American women,
hair. Blacks also have fewer elastic fibers anchor- characterized by scarring hair loss first seen on
ing hair follicles to the dermis. Conversely, Asian the vertex of the scalp.
hair is rounder, with the largest cross-sectional
area relative to other ethnicities, resulting in hair 2.2.1.2 Epidemiology
that is generally straighter [5, 6]. These variations CCCA is the most common scarring alopecia
account in part for the different clinical charac- among African American women and is rarely
teristics seen in the hair of these ethnic groups. reported in other ethnic groups. Large population
African Americans tend to have hair that is drier, based studies are lacking, but one study of African
slower growing and more fragile compared to American women in the Southeastern United
Caucasians. Conversely, Asian hair tends to be States found the incidence of CCCA to be 5.6%
thicker in diameter with faster growth [7, 8]. [9]. Although it is predominantly seen in women,
it has been reported in African American men [10].

2.1.2 Cultural Differences 2.2.1.3 Pathogenesis


CCCA is an inflammatory disorder which ulti-
Due to these physiologic differences, cultural dif- mately results in scarring; however, the specific
ferences exist in terms of how the SOC popula- reasons why this inflammation occurs remain
tion cares for their skin and hair. For example, elusive and are likely multifactorial.
African Americans may braid their hair in corn-
rows as a symbol of cultural identity and because Skin of Color
it offers a lower maintenance hairstyle. Hair Despite the fact that the specific pathogenesis of
extensions and weaves are used to give the hair a CCCA is unclear, one prevailing theory is that it
longer, straighter or more voluminous appear- is due in part to traumatic hair styling practices,
ance. Given the curly nature of Black hair, it is which are much more common in Blacks. These
also common for them to straighten their hair include tight braids, weaves, or cornrows and the
with chemicals or heat such as hot combs, flat use of chemical relaxers, texturizers, and/or heat.
irons and blow dryers. Alternatively, Sikh men Although this theory has been reinforced by stud-
and women do not cut their hair but rather allow ies in which a significant association between
it to grow as a symbol of devotion to God. They CCCA and hairstyling practices was observed,
also wear turbans to care for their hair and as a other studies were unable to find a similar asso-
sign of identity and equality. Over time, many of ciation [9, 11].
these hair styling practices can lead to irritation It has also been suggested that there is a
and follicular damage which propagates the genetic component to the development of CCCA,
inflammatory cascade. Ultimately, these different as it has been described to run in families. Dlova
physiologic and cultural differences have been et al. observed 14 South African families in
implicated in the pathogenesis of several diseases which an autosomal dominant pattern of CCCA
seen more commonly in skin of color. was demonstrated. Furthermore, 20% of these
2  Racial and Gender Influences on Skin Disease 13

individuals reported no history of traumatic hair- be started as soon as possible. It is important to


styling, which suggests that there is more to the discuss and set expectations with the patient,
pathogenesis of CCCA than these practices, and a including the fact that it is challenging to predict
genetic component may also be at play [12]. the course of the disease. Furthermore, if scarring
has already occurred, it is important to make the
Gender patient aware that regrowth will be quite limited.
Males rarely use the hair styling practices which Unless these expectations are outlined early and
have been implicated in the pathogenesis of CCCA, clearly, at future visits, patients may be frustrated
which may explain why it is far less common for with their management.
them to be affected. However, the fact that it has Given the implication of certain hair styling
been seen in males, particular African American techniques in the pathogenesis of CCCA, it
males, supports the claim that there may be an should be stressed to patients to avoid such prac-
underlying genetic component to the disease [10]. tices, even if they have denied using them in the
past. Being a disease of inflammation, topical or
2.2.1.4 Clinical Features intralesional steroids are typically used. Oral tet-
As the name suggests, CCCA generally begins on racyclines have also been used in the treatment of
the crown or vertex of the scalp, and slowly CCCA. Other therapies that have been reported
expands centrifugally. In early stages, mild hair anecdotally include antimalarials, topical calci-
thinning may make the disease difficult to distin- neurin inhibitors, minoxidil, thalidomide, cyclo-
guish from androgenetic alopecia. Although it sporine and mycophenolate mofetil [13].
typically expands slowly, it can eventually prog- Patients may present to clinic specifically
ress centrifugally to affect the entire crown of the inquiring about the effectiveness of hair trans-
scalp. Left untreated, scarring occurs and the scalp plantation, and in some cases may have already
becomes smooth and shiny, with follicular dropout consulted with a hair transplant surgeon.
and preservation of a few short, brittle hairs [13]. Although hair transplantation has been reported
Patients may complain of mild pruritus or ten- to be successful in patient who have had stable
derness in the area that is affected, which can be disease for at least 9–12 months, patients should
a sign of disease activity. In certain cases, patients be educated on the potential need for multiple
may present with superimposed folliculitis decal- hair transplant sessions, the need for continued
vans, with pustules and crusting. medical therapy, and the possibility of disease
recurrence [15].
2.2.1.5 Histology
Depending on the stage of the disease, CCCA
demonstrates a follicular lichenoid lymphocytic 2.2.2 Traction Alopecia
infiltrate when caught early, which leads to fol-
licular fibrosis as it progresses. Features that help 2.2.2.1 Introduction
make the diagnosis include follicular miniatur- Traction alopecia (TA) is another form of scar-
ization, premature desquamation of the inner root ring alopecia that is most prominently seen in
sheath, focal preservation of sebaceous glands, women of color. It develops in the setting of hair
naked hair shafts, compound follicular structures, styling techniques that create prolonged tension
perifollicular fibrosis and/or inflammation, and or repetitive pulling on hair.
lamellar hyperkeratosis and parakeratosis in the
hair canal [14]. 2.2.2.2 Epidemiology
TA is almost exclusively reported in women and
2.2.1.6 Treatment is most frequently seen in African Americans.
There are limited treatment options available for That said, it has also been described in other eth-
CCCA, and results are often unsatisfactory. As it nic groups, and the prevalence rate has also been
can ultimately lead to scarring, treatment should reported to be relatively high in Hispanics [16].
14 D. Callaghan and N. A. Vashi

Although it is far less commonly described in Although clinical history is crucial in making
males, they can also be affected; for example, TA this diagnosis, it is not uncommon for patients to
has been reported among Sikh males who wear deny styling their hair in a manner that predis-
their hair twisted tightly under turbans [17]. One poses them to TA. When the history does not sup-
study looking at 874 South African adults found port the diagnosis, the clinician may look for the
that 31.7% of women had TA compared with just fringe sign to help identify the disease. The
2.2% of men [18]. ‘fringe sign’ describes the presence of short
retained hairs along the hairline and can help dis-
2.2.2.3 Pathogenesis tinguish TA from other forms of hair loss such as
Traction alopecia develops when hairstyling ophiasis alopecia areata. It has been reported in
practices cause tension on the hair follicle, which up to 100% of women with TA affecting the fron-
over time leads to inflammation, fibrosis and per- tal or temporal hairlines [16].
manent alopecia.
2.2.2.5 Histology
Skin of Color Histologically, early TA demonstrates decreased
The increased prevalence of TA in Blacks is follicular number but preservation of the seba-
explained both by cultural and physiologic differ- ceous glands. Features of trichomalacia, includ-
ences. As described before, Black hair grows in a ing twisting or deformation of anagen bulbs can
tight spiral pattern, making it more susceptible to also be seen when caught early. Depending on the
breakage when manipulated. Furthermore, stage, follicular scarring may or may not be pres-
Blacks more commonly use hair styling tech- ent. As the disease progresses, the number of
niques such as braids, weaves, chemical relaxers sebaceous glands may be reduced and hair folli-
and heat, which puts more tension on their hair cles become surrounded by a lymphocytic infil-
and increases their risk of developing TA. For trate and fibrosis [20]. However, these findings
instance, it has been shown that chemically pro- are not pathognomonic and clinicopathologic
cessed hair has a greater risk of developing TA correlation is necessary to make an accurate
[19]. TA can also be seen in Hispanics who wear diagnosis.
their hair in tight ponytails. Japanese women
have also been reported to get TA on the occipital 2.2.2.6 Treatment
or temporal scalp from wearing their hair in a The first step in the treatment of TA is cessation
tight bun [16]. of any hairstyling technique which may be con-
tributing to the disease process. It may be diffi-
Gender cult to convince patients to change their
The increased prevalence in women is explained hairstyling practices, which they have often been
by the fact that they are far more likely to style using for years. As the hair styling practices that
their hair using the aforementioned practices. lead to TA are often started in childhood, it is
important to also educate parents about this risk
2.2.2.4 Clinical Features to help prevent the disease.
TA is most commonly seen in the frontal and In the setting of active inflammation, topical
temporal region of the scalp but can present or intralesional steroids can be used. Intralesional
anywhere depending on the hair styling prac- administration of steroids should be performed at
tice. When caught early, there may be perifol- the periphery of the hair line to prevent retained
licular erythema, papules or pustules. In a study hair from being lost. Oral antibiotics are also uti-
involving 41 patients with TA, including 12 lized in cases of TA when there is clinically
Hispanic patients, Samrao et al. reported clini- apparent inflammation.. With patients who have
cally evident inflammation in 54% of African lost hair as a result of TA but have not yet devel-
American women compared with 17% of oped scarring, topical minoxidil may be benefi-
Hispanic women [16]. cial [21].
2  Racial and Gender Influences on Skin Disease 15

As with other scarring alopecias that are diffi- intrafollicular canal or sebaceous glands.
cult to manage medically, camouflage techniques Antigens that have been implicated include nor-
can be effective and can help improve patients’ mal skin flora, demodex, desquamated keratino-
quality of life. Surgical options, including follic- cytes, sebum and cosmetics [27, 28]. This
ular unit transplantation and mini- or micrograft- inflammation results in damage to the hair shaft,
ing have also been reported to be effective in the with the resulting clinical changes described in
appropriately selected patient [22]. AKN. Other reported etiologic factors have
included seborrheic dermatitis, Staphylococcus
aureus infection, and elevated serum testosterone
2.2.3 Acne Keloidalis Nuchae levels [29].

2.2.3.1 Introduction Skin of Color


Acne keloidalis nuchae (AKN) is a form of Previously, AKN was thought to be the result of
chronic folliculitis most frequently seen in Black inward growth of hair leading to a foreign body
males. It is characterized by papules and pustules reaction and subsequent inflammation. The spi-
on the occipital scalp and posterior neck, which raled nature of hair in Blacks would make them
over time can develop into keloid-like plaques more susceptible and explains why they are more
and scarring alopecia. commonly affected by the disease. That being
said, there is no clinical or histologic evidence to
2.2.3.2 Epidemiology substantiate this claim. For instance, one South
AKN has been described in all races but is most African study did not find an association between
frequently seen in Black men after adolescence the prevalence of AKN and the use of clippers as
and under the age of 55. In decreasing incidence opposed to razors [18]. Furthermore, one author
it also affects Hispanic, Asian and Caucasian observed that ingrown hairs are not commonly
males [23]. Knable et al. studied 453 male foot- seen in AKN as they are in PFB [27, 30].
ball players between the ages of 14 and 27, and If this theory is to be disregarded, it is unclear
found that while AKN was seen in 24% of black why there is an increased prevalence of AKN in
players, no white players were affected [24]. Blacks. If one subscribes to the thought that AKN
Although 20 times more common in men, women is a primary cicatricial alopecia resulting from
can also be affected by it [25]. immune dysregulation, it may be that there is a
genetic component which predisposes these indi-
2.2.3.3 Pathogenesis viduals to the disease.
Despite its name, AKN is not a variant of acne
vulgaris, and the name folliculitis keloidalis Gender
nuchae has been suggested. The exact etiology is Similarly, our lack of understanding of the patho-
unknown, but it is a result of chronic inflamma- genesis of AKN makes it difficult to explain why
tion which ultimately leads to scarring and it is almost exclusively seen in males. However,
keloid-like plaques. that observation alone, coupled with the fact that
The development of AKN is typically attrib- it is rare before puberty or after the age of 55, has
uted to chronic trauma to the follicular scalp. led some to propose that there is a hormonal
Most investigators believe that AKN is a result of component involved. An increase in androgen
mechanical injury from friction and hair styling levels, androgen receptor sensitivity or increased
practices, such as the use of electric razors and activity of sebaceous glands may play a role [30].
shaving, which leads to irritation, occlusion,
trauma and inflammation [26]. 2.2.3.4 Clinical Features
Some propose that AKN is a primary cicatri- AKN initially presents as inflammatory papules
cial alopecia resulting from an immune response on the nape of the neck and posterior scalp, which
against antigens on the follicular epithelium, over time result in fibrosis and keloid-like
16 D. Callaghan and N. A. Vashi

plaques. These patients can also develop second- treatment option; however, the risk of scarring is
ary infection with pustules, subcutaneous an obvious concern. Unfortunately, the risk of at
abscesses and sinus drainage. Repeated inflam- least mild recurrence is nearly 50%, typically
mation leads to the destruction of hair follicles, within weeks to months of medication discontin-
fibrosis and ultimately scarring alopecia. uation [26].
Furthermore, the keloid-like plaques that develop
are usually devoid of hair.
These changes can be a significant cosmetic 2.2.4 Pseudofolliculitis Barbae
concern to patients and negatively affects their
quality of life [23, 31]. Similar to other inflam- 2.2.4.1 Introduction
matory disorders, these patients also complain of Pseudofolliculitis barbae (PFB) is a chronic, non-­
pruritus, and the lesions can be painful and tender infectious, inflammatory follicular disorder
to palpation. which results in erythematous papules most fre-
quently found in the beard area. Given the simi-
2.2.3.5 Histology larities in appearance of AKN and PFB, the two
Histologic characteristics of AKN include peri- diseases were previously thought to be on the
follicular, lymphocytic and plasmacytic inflam- same spectrum, with the difference being the
mation most intense at the level of the isthmus location they affected. However, the two diseases
and lower infundibulum, lamellar fibrosis, loss of are now thought to be separate entities, each with
sebaceous glands, thinning of the follicular epi- a different pathogenesis.
thelium and total epithelial destruction with
residual “naked” hair fragments [28]. These his- 2.2.4.2 Epidemiology
tologic findings closely resemble other forms of PFB is most often found in Black males, with the
cicatricial alopecia, which is what has led some reported incidence varying from 45% to 83%. It
to propose it to be a form of primary cicatricial is also seen in other populations who may have
alopecia. more tightly curled hair, including Hispanics and
Middle Easterners. It is less commonly observed
2.2.3.6 Treatment in women [32].
Early treatment correlates with a good prognosis;
however, as the disease progresses, it can be more 2.2.4.3 Pathogenesis
difficult to treat and more invasive measures must PFB occurs because of ingrown hairs, which
be utilized. induce a foreign body inflammatory reaction
Management is typically first directed at upon re-entering the skin through extrafollicular
avoiding any inciting factors that may be causing or transfollicular penetration. Certain hair styling
irritation. Mild disease can be managed medi- techniques, such as pulling the skin taut while
cally with topical or intralesional steroids, topical shaving and/or cutting the tip to a sharp point,
or oral antibiotics, particularly tetracyclines, and can make re-entry more likely.
retinoids [26].
Light and laser therapies, including the 1064-­ Skin of Color
nm neodymium-doped yttrium aluminum garnet Blacks have tightly spiraled hairs, which curve in
(Nd:Yag) laser and targeted UVB light, have such a manner to emerge almost parallel to the
offered promising results with mild side effects skin. Rather than continue to grow outward, this
including transient erythema and mild burning. orientation puts them at risk to curl and re-enter
These treatment options work to destroy the hair the skin. Beyond this, some individuals may have
follicle and decrease the inflammation implicated a genetic predisposition to developing PFB, which
in the pathogenesis of the disease. was demonstrated by Winter et al. who found that
Surgical or cryosurgical treatment with sec- a defect in a hair follicle keratin increased the risk
ondary intention healing may be an effective of developing PFB by a factor of 6.12 [33].
2  Racial and Gender Influences on Skin Disease 17

Gender electric shavers. However, that can be an incon-


PFB is thought to affect males more so than venience for individuals who prefer to be closely
females because of its close association with shaved, and is impractical for others who may be
shaving. That being said, women can also develop required to be closely shaved. For those who are
PFB. One study found that hormonal disorders able to stop shaving, remission is often seen
leading to hyperandrogenism and hirsutism is a within 30 days [36].
risk factor for women to develop PFB [34]. For men who are unable or unwilling to avoid
shaving, shaving techniques that have been pro-
2.2.4.4 Clinical Features posed to help reduce the burden of PFB include
PFB presents as firm, follicular or perifollicular shaving regularly to prevent hair from growing
papules most often found on the neck and cheeks long enough to re-enter the skin, preparing the
in men. Some papules may contain visible hairs. skin beforehand with warm water and a gentle
When it does affect women, the chin is the most cleanser to soften the hair, applying shaving foam
commonly area affected, especially in hirsute or gel to provide a protective anti-friction layer,
women who shave or pluck unwanted hairs. keeping the skin relaxed rather than pulling taut,
Although it is associated with shaving in men, it and using a technologically advanced multiblade
should be noted that the mustache and nuchal razor or foil-guarded manual single-blade razor.
areas are rarely affected [32, 35]. The use of after-shave products containing mois-
Although secondary infection can occur, pus- turizing ingredients also help rehydrate and com-
tules are rare in PFB, which can help distinguish fort the skin [35].
it from acne vulgaris. No comedonal lesions are For PFB that cannot be controlled by non-­
seen in PFB, which also helps distinguish it from medical interventions, retinoids have been
acne. reported to improve the disease, with the thought
PFB must also be distinguished from trau- that they relieve hyperkeratosis and remove the
matic folliculitis, more commonly known as thin covering of epidermis that the hair becomes
razor burn. Traumatic folliculitis occurs when embedded in when re-entering the skin. Mild
shaving is performed too closely. It presents as topical corticosteroids can also be used temporar-
painful follicular papules which may be confused ily to reduce inflammation [32]. In addition, topi-
for PFB but disappear within 24–48 h. PFB, con- cal eflornithine hydrochloride cream can be used
versely, persists for weeks after cessation of to slow hair growth.
shaving. For severe disease, especially in the setting of
PFB may be associated with pruritus and pain frequent superinfection with the development of
and may be complicated by postinflammatory pustules and abscess formation, topical or oral
hyperpigmentation (PIH), scarring, and forma- antibiotics may be indicated, with tetracyclines
tion of keloids [32]. commonly employed [35]. Laser therapy has
been used successfully, with the Nd:YAG
2.2.4.5 Histology 1064 nm lasers having the best safety and effi-
Histopathologically, PFB is characterized by a cacy profile for use in SOC patients.
foreign body inflammatory response to hair re-­
entering the skin. Epidermal penetration shows
invagination with an inflammatory infiltrate, 2.2.5 Dissecting Cellulitis
which becomes more intense as the hair reaches
the dermis [21]. 2.2.5.1 I ntroduction
Dissecting cellulitis of the scalp (DCS) is a form
2.2.4.6 Treatment of primary neutrophilic cicatricial alopecia. It is a
Given its pathogenesis, the first recommendation chronic inflammatory disorder resulting in scar-
in the management of PFB is often cessation of ring alopecia more frequently seen in Black
shaving, the only curative treatment, or use of males. It makes up a component of the follicular
18 D. Callaghan and N. A. Vashi

occlusion tetrad, which also includes hidradenitis erature, it suggests that there is a genetic risk fac-
suppurativa (HS), acne conglobata, and pilonidal tor, which may be predisposing Black patients to
cysts. the disease disproportionately [40].

2.2.5.2 Epidemiology Gender


DCS is most commonly seen in Black males It is also unclear why males are affected more pre-
between their third to fifth decades of life, with dominantly than females. Hormones have been
only 10% of cases involving Caucasians [37]. suggested to play a role in its pathogenesis, and
Although it can affect women, it is rare. A retro- one retrospective review found that 3/21 (14%) of
spective study of 51 patients with DCS in France patients associated the onset of their disease with
found that 65% were skin type IV or above, and use of anabolic-androgenic steroids [41].
only 1 was female [38]. One third of patients with
DCS have coexisting acne conglobata or hidrad- 2.2.5.4 Clinical Features
enitis suppurativa, and are thought to be at an Dissecting cellulitis typically begins as a follicu-
increased risk for developing HLA-B27 negative lar pustule on the occipital or vertex of the scalp.
spondyloarthropathy [21]. Patients may develop multiple pustules which
can evolve into nodules and abscesses that form
2.2.5.3 Pathogenesis interconnecting sinus tracts. Over time, if
The overlying pathogenesis of DCS is thought to untreated, the scalp takes on a cerebriform, boggy
be the result of a defect in follicular keratiniza- appearance with resulting overlying scarring alo-
tion, which leads to occlusion of the piloseba- pecia. This can be further complicated by hyper-
ceous unit and accumulation of sebaceous and trophic scarring and keloids. Patients’ quality of
keratinous material. This leads to subsequent fol- life can be severely affected as the lesions can be
licular expansion and inflammation. Dilated fol- both painful and disfiguring [4, 37, 39].
licles can rupture, further propagating the
inflammation with a neutrophilic and granuloma- 2.2.5.5 Histology
tous response. Secondary infection can occur Similar to other inflammatory, scarring diseases,
with the development of folliculitis. Ultimately, the histopathologic features of DCS demonstrate
chronic inflammation results in nodules and great variability based on the stage of the disease
abscesses which can form interconnecting sinus examined. In early lesions, dilatation of the
tracts and can also result in scarring and alopecia. infundibula is observed, with a surrounding peri-
These sinus tracts can serve as niduses for bacte- follicular, mixed, neutrophilic and lymphoplas-
rial overgrowth and inflammation, resulting in a macytic infiltrate, particularly affecting the lower
cyclical inflammatory and scarring process that portion of the infundibula. As the disease pro-
can be difficult to control [21, 39]. gresses, deep-seated abscesses in the adventitial
The inciting factor for this process has yet to dermis and subcutis form and follicular destruc-
be fully elucidated. One theory that has been pro- tion results, with eventual fibrosis. Sinus tracts
posed is it is the result of loss of immune toler- can be seen which are lined with squamous epi-
ance to alloantigens in the hair follicle, which thelium [42].
leads to the inflammatory response seen [38].
2.2.5.6 Treatment
Skin of Color Management of DSC remains challenging.
It is unclear why DCS is seen more frequently in Therapy is initially managed medically, with top-
Blacks. The role of hair type and hair styling ical or intralesional steroids, antibacterial cleans-
practices has also been suggested to be impli- ers, topical or oral antibiotics, prednisone and
cated in the pathogenesis of DCS; however, isotretinoin as monotherapy or in combination
strong evidence supporting this is sparse. As with rifampin. Although relapse is common after
there have been cases of familial DCS in the lit- discontinuation, there are some reports of isotret-
2  Racial and Gender Influences on Skin Disease 19

inoin causing a sustained remission for up to 0.034% of the Asian population is affected by
2.5 years [43]. TNF-α inhibitors, which have nevus of Ota, and it is five times more likely to be
been used to treat HS and acne conglobata, have seen in women than men [47, 48]. They have
been reported to show improvement in some been reported to be unilateral in 90% of cases and
patients with refractory DSC; however, not all bilateral in 5–10% of cases [48]. Dermal melano-
patients show a response [44, 45]. cytoses can be congenital or acquired. Nevus of
Resistant DCS has been successfully treated Ota is typically congenital; however, may appear
with laser therapy, including an 800 nm pulsed during puberty. When small lesions are acquired,
diode laser and the 1064 nm long-pulse Nd:YAG they are called Sun’s nevus if unilateral, and
laser [21]. Hori’s nevus if bilateral. A population-based
Though medical options can be valuable in sta- study in Taiwan described the overall incidence
bilizing the disease process, some feel they can of ABNOM to be 0.8% [46].
never offer a sustainable response as they are
unable to address the existing sinus tracts, which 2.3.1.3 Pathogenesis
serve as a nidus for infection, drainage, and con- Nevus of Ota is thought to be the result of migration
tinued inflammation. For this reason, severe dis- arrest of melanocytes on their way from the neural
ease has been treated with complete scalp excision crest to the epidermis [49]. It has been hypothesized
followed by split-thickness skin grafting, although that the acquired variant of these lesions may be
side effects and recurrence have been reported to related to reactivation of existing dermal melano-
occur. More recently, Powers et al. reported ben- cytes which were previously misplaced during
efit from a staged excision, which provides the embryological development [50]. One recent
benefits of more targeted focus of disease control review of 102 patients found sun exposure (47.1%),
and preservation of hair-­bearing portions of the pregnancy (32.0%), cosmetics (29.4%), sensitive
scalp, leading to better outcomes [37, 39]. skin (22.6%) and positive family histories (21.6%)
to be highly related to the development of ABNOM
[51]. Given the higher prevalence among Asians, a
2.3 Disorders of Pigmentation genetic component likely exists. It has also been
suggested that hormones play a role in the patho-
2.3.1 Nevus of Ota genesis as pregnancy has been associated with the
development of ABNOM.
2.3.1.1 Introduction
Dermal melanocytoses comprise a group of 2.3.1.4 Clinical Features
melanocytic lesions which can be congenital or Nevus of Ota presents as a bluish or gray-brown
acquired. Nevus of Ota, acquired bilateral nevus discoloration in areas innervated by the first two
of Ota-like macules (ABNOM, also known as branches of the trigeminal nerve. Roughly two-­
Hori’s nevus) and acquired unilateral nevus of thirds of patients will have characteristic involve-
Ota-like macules (also known as Sun’s nevi) are ment of the ipsilateral sclera.
three facial dermal melanocytoses which are far ABNOM present as blue-brown and/or slate-­
more commonly found in Asian females. gray macules occurring in a speckled pattern
Controversy exists as to whether or not these bilaterally on the malar regions, and can also
lesions belong on a spectrum or are clinically involve the forehead, upper eyelids, cheeks and
separate entities [46]. Histology and treatment of nose [46]. Although some consider these lesions
all lesions are similar. to be on the same spectrum of Nevus of Ota, oth-
ers distinguish them by their adult onset, speck-
2.3.1.2 Epidemiology led and bilateral pattern, and lack of mucosal
Nevus of Ota primarily affects Asian populations involvement [52].
but can also be seen in Africans and Indians. It is Patients with nevus of Ota are at increased risk
rarely seen in Caucasian patients. Approximately for glaucoma, and therefore should be followed
20 D. Callaghan and N. A. Vashi

with routine eye exams [53]. Malignant transfor- a complex interplay of genetics, hormones, and
mation of dermal melanocytoses is rare. A recent exposure to ultraviolet and visible light.
review found a total of 14 cases of cutaneous
melanoma arising in dermal melanocytoses, with 2.3.2.2 Epidemiology
10 of those arising within nevi of Ota, and 4 aris- The prevalence of melasma varies widely based
ing within nevi of Ito. Interestingly, of the 10 on the ethnic and geographic composition of the
reported cases of cutaneous melanoma arising in population. When populations of skin of color
association with nevus of Ota, 8 of the patients have been studied, the prevalence of melasma has
were Caucasian, with the race/ethnicity of the ranged from 8.8% to 41% [57]. Most studies
two additional patients not being reported [54]. report the incidence of melasma being highest in
Although asymptomatic, as nevus of Ota can be skin types III–V. It predominantly affects women,
cosmetically disfiguring, patients can suffer from with one population based study out of Brazil
severe emotional or psychological distress [47]. reporting it in 6% of men [58].

2.3.1.5 Histology 2.3.2.3 Pathogenesis


Lesions demonstrate irregularly shaped melano- Pathophysiology remains unclear. Ultraviolet
cytes dispersed throughout the dermis. and visible light exposure, pregnancy, sex hor-
mones, use of oral contraceptives, steroids,
2.3.1.6 Treatment inflammation and photosensitizing drugs are
As with other pigmentary disorders, photoprotec- known triggers that have been implicated in its
tion is a cornerstone of therapy. Cosmetic camou- pathogenesis. In addition, melanocytes associ-
flage may also be utilized to help reduce the ated with melasma lesions are more biologically
burden of disease. Laser therapy is the treatment active when compared to normal skin; this is evi-
of choice for nevus of Ota. Traditionally denced by increased mitochondria, Golgi com-
Q-switched (QS) lasers, including the 694 nm QS plex, and rough endoplasmic reticulum [59]. The
ruby, 755 nm QS alexandrite, and both the 532 growing knowledge on melasma pathogenesis
and 1064 nm QS Nd:YAG lasers showed the suggests a complex cellular interplay involving
most favorable clearance rates with the fewest melanocytes, keratinocytes, dermal fibroblasts,
side effects [47]. increased vascularity and increased mast cells.
More recently, picosecond lasers have been
shown to be safe and effective in the treatment of Skin of Color
these lesions [55]. Although not all lesions Although melasma is found in all ethnic groups,
respond to treatment, but for those that do studies have shown a higher prevalence in more
respond, recurrence rate after treatment is rare pigmented populations including Hispanic,
(0.8–2.1%) [56]. When the appropriate patient Japanese, Korean, Chinese, Indian, Pakistani,
and laser are selected, side effects are infrequent; Middle Eastern, and Mediterranean-African indi-
however, risk of post-inflammatory hyperpig- viduals [60, 61]. It may also be seen more in
mentation should always be considered in the these populations because of a genetic influence,
SOC population. which has been theorized based on its tendency
to run in families, with over 40% of patients
reporting having relatives affected with the dis-
2.3.2 Melasma ease [57].

2.3.2.1 Introduction Gender


Melasma is a common disorder of hyperpigmen- There is a clear association between hormones
tation with higher prevalence in females along and the development of melasma as it is most
with Fitzpatrick skin types III–IV and/or those of commonly seen among women and with the use
Hispanic descent. It is thought to be the result of of oral contraceptives and during pregnancy.
2  Racial and Gender Influences on Skin Disease 21

Despite this strong association, the specific role of melasma after beginning oral contraceptives,
hormones play in its pathogenesis is poorly they should be stopped if possible [52]. Topical
understood. However, it is known that human agents including hydroquinone, retinoids and
melanocytes have estrogen and progesterone azelaic acid have been reported with good suc-
receptors, and the expression of estrogen recep- cess in the treatment of melasma. Combination
tors appears to be increased in skin affected by creams have been shown to be more successful
melasma [62, 63]. than monotherapy [66].
Chemical peels may be useful for patients
2.3.2.4 Clinical Features with moderate to severe melasma that is resis-
Melasma presents as hyperpigmented macules tant to topical therapy. Superficial peels, includ-
coalescing into irregularly shaped patches most ing glycolic acid and salicylic acid peels, have
commonly found on the cheeks, upper lip, fore- been shown to be effective with few adverse
head, nose, cheek and chin. Extra-facial disease effects [67].
on sun-exposed areas can also occur. Under der- Laser and light based therapies, including
moscopy, when limited to the stratum corneum intense pulsed light, QS Nd:YAG and pulse dye
melasma presents as a well-defined brown to lasers, have been shown to be effective in severe
dark brown network. When it involves the lower or refractory disease. These therapies are limited
epidermis, it appears as lighter shades of brown by the fact that they demonstrate a high relapse
with a more irregular network. When there is also rate and carry the risk of side effects including
involvement of the dermis, it demonstrates a blue PIH, particularly in darker skin types [66]. Newer
or bluish-gray color [57]. lasers, such as those using picosecond technol-
Melasma can cause a significant amount of ogy, show promising results and limited side
psychological stress in patients and negatively effects.
affects their quality of life [64]. Oral agents have been used for the treatment
of melasma, with oral tranexamic acid showing
2.3.2.5 Histology the most promising results [68, 69]. Other agents
Melasma is characterized by hypertrophic mela- with a good safety profile that may have efficacy
nocytes and an increased amount of melanin seen include Polypodium leucotomos extract, carot-
in all layers of the epidermis along with a possi- enoid, melatonin and procyanidin. However,
ble increased number of melanophages. An these agents are most commonly used as supple-
increased number of melanocytes are not ments to other treatments options and are rarely
observed [59]. considered to be effective as monotherapy.

2.3.2.6 Treatment Conclusion


There are a wide variety of treatment options for Differences in cultural practices, particularly
melasma, and while many patients respond favor- hair styling practices, as well as physiologic dif-
ably, it can be resistant to treatment in others. ferences, such as an increased amount of mela-
Treatment is aimed at reducing the amount of nin, are implicated in many of the dermatologic
epidermal melanin and blocking solar radiation. conditions that are more commonly seen in skin
Melasma that is seen more intensely under of color. Similarly, differences in hair styling
Wood’s lamp examination typically responds practices between men and women, as well as
better to topical treatments [57]. differences in hormone levels, may explain why
The mainstay of treatment for melasma is pre- there is a discrepancy in the incidence of some
ventative therapy, including strict photoprotec- diseases in different genders. More research
tion with sunscreen and sun avoidance. This is must be performed to further illustrate the
especially valuable to reinforce in this patient pathogenesis behind these conditions, which
population, that may not be accustomed to wear- will allow for more targeted and effective treat-
ing sunscreen [65]. In women who note the onset ment options. Skin of color represents an incred-
22 D. Callaghan and N. A. Vashi

ibly heterogeneous group of individuals, and J Am Acad Dermatol. 2014;70(4):679–82. https://doi.


care must be taken to avoid making generaliza- org/10.1016/j.jaad.2013.11.035.
13. Herskovitz I, Miteva M. Central centrifugal cicatri-
tions about patients, but rather each patient must cial alopecia: challenges and solutions. Clin Cosmet
be treated individually for optimal results. Investig Dermatol. 2016;9:175–81.
14. Miteva M, Tosti A. Dermatoscopic features of cen-
tral centrifugal cicatricial alopecia. J Am Acad
Dermatol. 2014;71(3):443–9. https://doi.org/10.1016/j.
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Aging of the Skin
3
Enzo Berardesca, Norma Cameli, and Maria Mariano

Skin aging is generally classified as intrinsic smoke, (4) nutrition, (5) a number of less well
aging and photoaging based on the mechanism of studied, miscellaneous factors, as well as (6) cos-
action and the skin site [1]. Intrinsic aging is metic products [6]. Basically all these damage epi-
characterized by thinning of the epidermis and dermal living cells and metabolism by increasing
fine wrinkles caused by cellular aging [1, 2], reactive oxygen species formation (ROS) inducing
while photoaging is characterized by deep wrin- changes in cell metabolism and function.
kles, skin laxity, telangiectasias, and appearance From a clinical point of view an important
of lentigines, and is mainly caused by exposure to change is the thinning of the epidermis. Starting
UV and other environmental factors [1, 3]. At the at about age 30, the epidermis decreases in thick-
cellular level skin aging has been attributed to the ness at about 6.4% per decade [7]. Changes in
loss of mature collagen and increased matrix epidermal thickness are most pronounced in
metalloproteinase (MMP) expression [1–3]. exposed areas, such as the face, neck, upper part
MMP-1 is known as an initiator collagenase of the chest and the extensor surface of the hands
responsible for collagen fragmentation in skin and forearms [8] due to the accumulation of
aging process, and MMP-2 and -9 are known to intrinsic aging and extrinsic aging. Flattening of
be responsible for further degradation of collagen the dermal–epidermal junction due to a retraction
[1, 3]. Impaired TGF-β signaling caused reduc- of the rete pegs is also a feature of aged skin [7].
tion of collagen synthesis is another reason for The skin becomes less resistant to shearing forces
collagen loss in aged skin [2, 4, 5]. and more vulnerable to insult [9]. Changes in
More recently, other environmental factors microcirculation and blood supply can be respon-
have been recognized being involved in the aging sible decreased basal cell proliferation and altera-
process known as the ‘exposome’ concept; it is tions in transcutaneous penetration [7, 10] With
generally agreed that both external and internal aging, epidermal turnover diminishes resulting in
factors as well as the response of the human body a smaller number of cell layers [11].
to these factors all add up to define the exposome.
Specifically, these can be conducted to: (1) sun
radiations: ultraviolet radiation, visible light and 3.1  hanges in Stratum
C
infrared radiation, (2) air pollution, (3) tobacco Corneum with Age

The water content of the SC decreases progres-


E. Berardesca (*) · N. Cameli · M. Mariano sively with age and eventually falls below the
San Gallicano Dermatological Institute, Rome, Italy level necessary for effective desquamation. This
e-mail: berardesca@berardesca.it

© Springer International Publishing AG, part of Springer Nature 2018 25


E. Tur, H. I. Maibach (eds.), Gender and Dermatology,
https://doi.org/10.1007/978-3-319-72156-9_3
26 E. Berardesca et al.

causes corneocytes to pile up and adhere to the time of the stratum corneum associated with
skin surface, which accounts for the roughness, increasing age [18]. The lengthening of the turn-
scaliness and flaking that accompanies xerosis in over implies a reduction in the desquamation
aged skin. The integrity of the SC barrier is rate but this is not as large as thought. The reason
dependent on an orderly arrangement of critical for this is the increase of corneocyte size during
lipids [7]. The total lipid content of the aged skin ageing. Thus there are fewer corneocytes in an
decreases dramatically, and this alteration in the old individual’s stratum corneum compared to a
lipid barrier results in dryer skin [12]. Age-related young one per volume unit. Studies measuring
changes in the amino acid composition reduce the release of corneocytes from the skin showed
the amount of cutaneous NMF, thereby decreas- also that there is a decrease of corneocyte loss at
ing the skin’s water-binding capacity [13]. least measured under these experimental condi-
There have been few attempts to measure the tions [19].
rate of corneocyte loss and desquamation in rela- The evolution of corneocyte size during the
tion with the ageing process. This is odd because ageing process has been studied by several
desquamation is a very important process. authors; there is a consensus that the size pro-
Corneocyte size and renewal (or turnover) gressively increases with age, even though there
depends not only by the rate of input into the are body site variations and seasonal variations
system (epidermopoiesis) but also on the rate at (changes due to hormonal status will be discussed
which cells are lost (desquamation). The epider- later in this document). The more investigated
mis shows a linear decrease in thickness with sites are the arm and the forearm and data shows
age, both in absolute terms and in cell number. a progressive increase of corneocyte size from
The reduction in epidermal population size sug- birth to age [20–23].
gests that there may be also a decrease in the rate Some differences have been reported between
on production of epidermal cells, and the appar- sunexposed and non sunexposed areas [24] where
ent lengthening of the stratum corneum renewal in general UV irradiation increases epidermal
time seems to confirm it. In addition, there is turnover leading to smaller corneocytes com-
some evidence that the rate of reepithelization of pared to a similar photoprotected site. Indeed,
wounds decreases with age. Using tritiated thy- seasonal variations in corneocyte size have been
midine and an autoradiographic labelling method reported with smaller corneocytes in summer as a
Kligman [14] reported a reduced value for an consequence of prolonged solar irradiation [25].
elderly cohort compared to a younger group; in a In a study on professional cyclists it was found
study comparing the effects of ageing between that the size of corneocytes from the area of the
sun exposed and non exposed sites this has not arm protected by the shirt was “normal”, while in
been detected [15]. In a more sensitive but com- the adjacent exposed area the area of the cells
plicated assay using the FACS fluorescent assay was significantly smaller [26].
it was demonstrated an age related decrease in In conclusion there is a correlation and an
the DNA synthesis and so in a longer cell cycle inverse relationship between stratum corneum
through the stratum corneum [16]. Stratum cor- turnover and dimensions of corneocytes.
neum cell turnover and replacement time have
been evaluated using also the dansyl chloride
staining technique. Dansyl chloride is a fluores- 3.2  hanges in the Dermis
C
cent dye which penetrates the full thickness of with Age
the stratum corneum and, when applied topically
to the skin in vivo, becomes florescent under At the dermal level, all three major extracellular
Wood’s light [17]. The time the fluorescente components of the dermis (collagen, elastin, and
takes to disappear corresponds to the turnover hyaluronic acid) are depleted in older skin.
cycle of the stratum corneum; these studies have Collagen content decreases at about 2% per year
shown a progressive increase in the turnover [27], due to both a decrease in collagen synthesis
3  Aging of the Skin 27

[28] and an increase in the degradation of colla- with premenopausal women [37]. Women with a
gen [29]. The relative proportions of collagen premature menopause have accelerated degener-
types are also disrupted in aged skin. The propor- ative changes in dermal elastic fibers [33]. In
tion of Type I collagen to Type III collagen in addition, decreased estrogens after menopause

Источник: https://www.scribd.com/document/454978907/Gender-and-Dermatology-by-Ethel-Tur-Howard-I-Maibach-eds-z-lib-org-pdf

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Gender and Dermatology by Ethel Tur, Howard I. Maibach (Eds.) PDF

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Dermatology

Ethel Tur
Howard I. Maibach
Editors

123
Gender and Dermatology
Ethel Tur  •  Howard I. Maibach
Editors

Gender and Dermatology


Editors
Ethel Tur Howard I. Maibach
Tel Aviv University Department of Dermatology
Tel Aviv UCSF Medical Center
Israel San Francisco
CA
USA

ISBN 978-3-319-72155-2    ISBN 978-3-319-72156-9 (eBook)


https://doi.org/10.1007/978-3-319-72156-9

Library of Congress Control Number: 2018936629

© Springer International Publishing AG, part of Springer Nature 2018


This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or
part of the material is concerned, specifically the rights of translation, reprinting, reuse of
illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way,
and transmission or information storage and retrieval, electronic adaptation, computer software,
or by similar or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this
publication does not imply, even in the absence of a specific statement, that such names are
exempt from the relevant protective laws and regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in
this book are believed to be true and accurate at the date of publication. Neither the publisher nor
the authors or the editors give a warranty, express or implied, with respect to the material
contained herein or for any errors or omissions that may have been made. The publisher remains
neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Printed on acid-free paper

This Springer imprint is published by the registered company Springer International Publishing
AG part of Springer Nature
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Preface

The nature of certain diseases is different between women and men. Genetic
and hormonal differences affect skin structure and function, thus affecting
disease processes. In addition, exogenous factors differ according to differ-
ences in lifestyle between the sexes. In the last two decades it has been recog-
nized that women are more different medically than previously appreciated,
and studies started being conducted accordingly. Methodologies used in der-
matological research have improved substantially, providing means of objec-
tive evaluation of skin function and characteristics, leading to improvement
in treatment and disease outcome.
Diseases differ between men and women in terms of prevention, clinical
signs, therapeutic approach, prognosis, and psychological and social impacts.
This book outlines several aspects of differences between the skin of
women and men in health and disease, based on available data. It is not
designed to be exhaustive in its coverage of the subject, but rather to highlight
certain aspects of it. We wish and hope that this book will ignite more interest
in the topic of gender dermatology.
The editors are grateful to all our contributing authors for their efforts and
cooperation in applying their knowledge and skill.
Special thanks to our team at Springer: Mr. Grant Weston, Responsible
Editor, Mr. Andre Tournois, Project Coordinator, Mr. Karthik Periyasamy,
Production editor, and Mr. Dinesh Vinayagam, Project Manager, for their
meticulous work.

Tel Aviv, Israel Ethel Tur


San Francisco, CA, USA Howard I. Maibach

v
Contents

1 Effects of Gender on Skin Physiology


and Biophysical Properties. 1
Richard Randall Wickett and Greg G. Hillebrand
2 Racial and Gender Influences on Skin Disease. 11
Daniel Callaghan and Neelam A. Vashi
3 Aging of the Skin. 25
Enzo Berardesca, Norma Cameli, and Maria Mariano
4 Hair and Scalp Variation Related to Gender. . 31
Ferial Fanian and Alexandre Guichard
5 Nail Variations Related to Gender. . 43
Robert Baran and Doug Schoon
6 Cutaneous Autoimmune Connective Tissue Disorders. . 53
Wohl Yonit
7 Gender Differences in Psoriasis. 63
Sivan Sheffer Levi and Yuval Ramot
8 Gender Dermatology: Pigmentation Disorders. 83
Mor Pavlovsky
9 Gender and Genodermatoses. . 89
Sivan Sheffer Levi and Vered Molho-Pessach
10 Specific Dermatoses of Pregnancy. . 127
Arieh Ingber
11 Nipples: A Sensitive Topic. . 139
Eve Finkelstein, Deena Yael Meerkin, and Gina Weissman
12 Acne Vulgaris.   171
Gila Isman Nelkenbaum
13 Melanocytic Nevi: Patterns and Gender Differences. 181
Miryam Kerner
14 Clinical and Therapeutic Considerations of Acquired
Melanocytic Nevi. 189
Baruch Kaplan

vii
viii Contents

15 Biology and Sex Disparities in Melanoma Outcomes. 193


Adi Nosrati and Maria L. Wei
16 Infantile Hemangioma. 215
Shoshana Greenberger
17 Cutaneous Leishmaniasis. . 227
Michal Solomon and Eli Schwartz
18 Fungal Infections (Onychomycosis, Tinea Pedis,
Tinea Cruris, Tinea Capitis, Tinea Manuum,
Tinea Corporis, different Candida Infections,
and Pityriasis Versicolor) and Mycological
Laboratory Analyses. . 235
Avner Shemer and Meir Babaev
19 Atopic Dermatitis. 243
Vered Atar-Snir
20 Occupational Dermatitis in Nail Salon Workers. . 249
Liran Horev
21 Universal Concepts of Beauty and Their Implications
on Clinical Approach to Female Cosmetic Patient. . 255
Marina Landau
22 Gender Differences in Mohs Micrographic Surgery. 267
Yoav C. Metzger
23 Gender Differences in Facial Rejuvenation. . 271
Benjamin C. Garden and Jerome M. Garden
24 The Skin as a Metaphor: Psychoanalytic
and Cultural Investigations. 281
Shlomit Yadlin-Gadot and Uri Hadar
Index.   299
Effects of Gender on Skin
Physiology and Biophysical 1
Properties

Richard Randall Wickett and Greg G. Hillebrand

Abbreviations corneum (SC) hydration measured by electrical


properties, skin viscoelasticity and facial skin
N.S. No significant difference wrinkling.
SC Stratum corneum
TEWL Transepidermal water loss
1.2 Sebum Production

On average sebum production is approximately


1.1 Introduction Microsoft Office 2013 Free Download same between men and women up to about
age 50. However, there is extreme variability
This chapter will review the literature on gender between individuals. Pochi et al. measured sebum
differences in skin physiology focusing on non-­ production rates in men and women between the
invasive biophysical measures of skin function. ages of 40 and 79 over a three-hour period using
While there are countless studies on the biophys- absorbent paper on the forehead [1]. Results are
ical properties of human skin, there are fewer presented in Table 1.1.
that examine gender differences. Many studies Sebum production clearly drops off in women
are sponsored by the cosmetic industry and not after age 50 probably because of menopause. In
surprisingly focus on women and often compare all age groups, even 70–79, there was consider-
effects of aging or photoaging. Unfortunately, able overlap between the ranges measured with
the literature that explores gender differences higher Filmora 8.2 Licensed email and Registration code producing women producing more
does not always present a clear picture as will be sebum in 3 h than lower producing men.
seen. This contribution will review sebum pro- A more bitdefender total security 2018 - Crack Key For U study of gender differ-
duction, skin pH, barrier function as assessed by ences in skin sebum production is that by
transepidermal water loss (TEWL), stratum Luebberding et al. [2]. The authors investigated
300 women and men between the ages of 20 and
74. Sebum production was measured on the
R. R. Wickett (*)
James L. Winkle College of Pharmacy, cheeks and foreheads using the Sebumeter [3].
University of Cincinnati, Cincinnati, OH, USA Mean values and standard deviations and statisti-
e-mail: wicketrr@ucmail.uc.edu cal significance levels (p values) for each age
G. G. Hillebrand Articulate Storyline Crack 3.11.23355.0 + Activation Code [Latest] range and over the entire age range are given in
Global Discovery, Research and Development, Table 1.2. There were 30 subjects of each sex in
Amway Corporation, Ada, MI, USA each age range.
e-mail: greg.hillebrand@Amway.com

© Springer International Publishing AG, part of Springer Nature 2018 1


E. Tur, H. I. Maibach (eds.), Gender and Dermatology,
https://doi.org/10.1007/978-3-319-72156-9_1
2 R. R. Wickett and G. G. Hillebrand

Table 1.1  Sebum production rates and ranges in female and male subjects
Age range Number F/M Femalea Rangea Malea Rangea
40–49 31/50 1.86 0.12–4.80 2.39 0.54–5.14
50–59 21/14 1.08 0.07–2.38 2.43 1.05–4.36
60–69 18/14 0.88 0.22–1.62 2.42 0.83–4.95
70–79 12/13 0.85 0.33–2.19 1.69 0.63–3.23
Sebum production in mg/10 cm2 of skin in 3 h data from Pochi et al. [1]
a

Table 1.2  Sebum levels on the forehead for females and trode at the skin surface with a hydrated skin-­
males
electrode interface [5]. In healthy skin, surface
Age range Femalea SD Malea SD p pH is lower than physiological pH ranging from
20–29 115.50 57.13 120.77 50.24 NS about 4.5–5.5 on most body sites under most con-
30–39 114.82 63.60 127.53 53.87 NS ditions. There has been increasing interest in the
40–49 130.77 63.74 125.93 50.27 NS
role of skin surface pH in maintaining a healthy
50–59 96.73 61.25 125.93 59.66 <0.05
stratum corneum barrier [5].
60–74 66.89 43.68 139.10 66.84 <0.001
Measurements of gender differences in skin
20–74 105.45 61.66 105.45 61.66 <0.001
pH have not produced completely consistent
a
Sebum measurement in μg/cm2 data from Luebberding
et al. [2]
results though there is a trend for females to have
slightly higher pH than males. Table 1.3 shows a
summary of results from several labs comparing
While the overall mean was smaller for the skin surface pH in men vs. women at various
women than men, significant differences were body sites and age groups. Table 1.3 doesn’t pres-
not seen before the 50–59 age group in agree- ent specific pH values because in some cases the
ment with the results of Pochi et al. above. Note authors only provide graphical data so exact
the large standard deviations indicating the large numerical values are not available. Luebberding
variation in sebum production across the sample et al. present numerical pH data and found that
populations. Sebum production on the cheek was males have significantly lower pH on every body
lower than on the forehead but age and sex differ- site for every age group [2]. The overall averages
ences showed very similar trends. Firooz et al. were 5.12 for females and 4.58 for males. This
[4] also reported lower sebum production in was among the largest differences seen in any of
females compared to males in pooled data from the papers reviewed. Zlotogorski [6] found 5.1
several age groups and body sites. Among all on the cheek for males and 5.2 on the cheek for
the skin parameters reviewed in this work, females and the difference was not statistically
lower sebum production in females compared significant. In contrast Ehlers and Ivens [7]
to males above the age of 50 was observed most reported higher skin pH in males (5.8) compared
consistently. to females (5.5) on the forearm.
In a large cross-sectional study of skin condi-
autocad 2020 crack download - Free Activators tion, Hillebrand and colleagues measured cheek
1.3 Skin Surface pH xlstat 2018 free download - Activators Patch and forearm skin surface pH in 450 subjects (191
males, 259 females) ranging in age for 9–78. The
pH is defined as ‘the negative logarithm of the subjects were art festival goers (ArtPrize 2015,
hydrogen ion concentration’. The most common Grand Rapids Michigan) who happened to walk
method for measuring the skin’s surface pH is to by the study venue and volunteered to be partici-
apply a flat surface membrane electrode hydrated pants. Thus, subjects were literally recruited off
with distilled water to the skin surface and mea- the street and represent a real world sampling of
sure the apparent pH. This leads to the definition the local population. Furthermore, the skin was
of skin surface pH in bioengineering terms as: not washed or prepared in any manner prior to
‘apparent pH as measured by a flat glass elec- making the measurement in order to measure an
1  Effects of Gender on Skin Physiology and Biophysical Properties 3

Table 1.3  Skin pH results from various authors


Age range Number F/M Body site Result Reference
20–60 292/282 Forehead M = F Zlotogorski [6]
20–60 292/282 Cheek M = F Zlotogorski [6]
21–37 37/46 Face M < F Kim [8]
13–70 354/304 Forehead M < F Man [9]
0–12 142/128 Forearm nVIDIA GeForce Experience Offline Installer M < F Man [9]
36–50 82/60 Forearm M < F Man [9]
51–70 28/31 Forearm M < F Man [9]
70+ 31/24 Forearm M = F Man [9]
70+ 31/24 Forehead M = F Man [9]
20–74 150/150 Forehead M < F Luebberding [2]
20–74 150/150 Cheek M < F Luebberding [2]
20–74 150/150 Neck M < F Luebberding [2]
20–74 150/150 Forearm M < F Luebberding [2]
20–74 150/150 Hand M < F Luebberding [2]
Not reported 6/6 Forearm M > F Ehlers [7]
9–78 259/191 Forearm M < F Hillebranda
9–78 259/191 Cheek M = F Hillebranda
a
G. G. Hillebrand unpublished data

unadulterated apparent pH. Skin pH ranged as have investigated possible gender differences


low as pH 3.1 to as high as pH 6.8 or nearly 4 in TEWL with varying results. Some of the
orders of magnitude in hydronium ion concen- results are presented in Table 1.4. Luebberding
tration! While there was no significant gender- et al. [2] reported higher TEWL in males than
dependent difference in cheek skin pH in females with significant differences on the
(mean ± SD: 5.28 ± 0.43 for males and forehead, cheek, neck and forearm. Chilcott
5.23 ± 0.47 for females), males showed signifi- and Farrar [12] reported higher TEWL in
cantly (p < 0.001) lower forearm skin pH com- males compared to females on the forearm and
pared to females (mean ± SD: 4.59 ± 0.61 for Firooz et al. [4] also reported higher TEWL in
males vs. 4.78 ± 0.65 for females). Figure 1.1 males in pooled data from eight body sites.
shows the percentage of males and females in Wilhelm et al. [13] and Hadi et al. [14] did not
specific pH ranges from pH 3 to pH 7. Females observe any significant effect of gender on
tend to skew to higher pH in accord with the dif- TEWL.
ference in the population means. What is note- Chilcott and Farrar [12] used the ServoMed
worthy is the large overlap in the wide bell EP-2 Evaporimeter (ServoMed, Kinna,
curves for skin pH frequencies between males Sweden) to measure TEWL while Luebberding
and females. Thus, the difference in mean pH et al. [2] used the TEWAmeter® TM300
between genders is small compared to the vari- (Courage & Khazaka, Cologne, Germany).
ance microsoft office click to run disable - Crack Key For U the entire population (Hillebrand, This may in part explain the higher forearm
unpublished data). results seen by Luebberding. While results
from the two instruments correlate very well,
TEWAmeter data tend to be up to two times
1.4 Transepidermal Water Loss higher than ServoMed data [11, 15]. Li et al.
[16] also reported lower TEWL in female sub-
Measurement of TEWL [10] has been shown jects compared to males in Chinese subjects
to be a valid method to evaluate skin barrier from two age groups, 18–25 and 40–50 on vari-
function in-vivo [11]. Several researchers ous body sites.
4 R. R. Wickett and G. G. Hillebrand

Fig. 1.1  Percent of 40


subjects (frequency %)
having forearm pH Males (n=191)
values in a specific pH Females (n=259)
range
30

Frequency % 20

10

0
0

.5

.0
0

7.
4.

4.

5.

6.

6.
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Forearm pH Range

Table 1.4  TEWL females and males


Ages No. (F/M) Body site Female Male P Reference
20–74 150/150 Forehead 10.51 9.29 Adobe After Effects CC Serial Number P < 0.01 Luebberding [2]
20–74 150/150 Cheek 11.15 10.34 P < 0.05 Luebberding [2]
20–74 150/150 Neck 9.25 6.96 P < 0.001 Luebberding [2]
20–74 150/150 Forearm 9.10 5.50 P < 0.001 Luebberding [2]
20–74 150/150 Hand 11.52 10.92 N.S. Luebberding [2]
18–28 10/8 Forearm 4.68 4.98 P < 0.05 Chilcott [12]
10–60 25/25 8 sites Vit Registry Fix Pro 12.6.6 Free Download with Crack 15.49 P < 0.05 Firoz [4]
N.S. no significant difference

1.5 Stratum Corneum Hydration Table 1.5  Capacitance by body site and gendera
Body site Female Male P value
The stratum corneum needs to maintain proper Forehead teamviewer software 52.94 50.94 N.S.
hydration in order to function properly and lack of Cheek 60.81 57.62 P < 0.05
adequate moisture in the SC can lead to dry skin. Neck 54.34 59.62 P < 0.001
Instrumental methods to measure SC hydration Forearm 44.07 43.10 N.S.
in-vivo rely on measuring either surface conduc- Hand 38.62 32.49 P < 0.001
tance or capacitance [17–20]. Luebberding et al. a
Data from Luebberding et al. [2]. 150 subjects of each
[2] measured skin hydration with the CM 825® sex in each age group. Age range = 20–74. N.S. no signifi-
cant difference
(Courage & Khazaka, Cologne Germany) on five
body sites on 150 subjects of each gender broken
into five age groups. Results from each body site, were not statistically significant. Li et al. [16] found
pooled by age are presented in Table 1.5. females to haves significantly higher hydration on
Females showed higher hydration on the cheek the décolletage are but no other body sites. Neither
and hand while males had higher values on the Firooz et al. [4] nor Wilhelm et al. [13] reported
neck. Differences on the forehead and forearm significant gender differences in hydration.
1  Effects of Gender on Skin Physiology and Biophysical Properties 5

1.6 Elasticity MPA 580 to measure skin elasticity in 25 females


and 25 males ages 10–60. While women had
Skin is a viscoelastic material. It has the unique slightly higher elasticity than men, the difference
ability to rebound after being stretched allowing was not statistically significant. More recently,
itself to return to its initial size and maintain a Hadi et al. [14] used the DermaLab® Combo to
tight covering over the body surface. measure the skin elasticity on the forearm of 50
Unfortunately, skin elasticity declines after the males and 50 females, ages 18–27. Females
third decade in both men and women, especially showed slightly higher skin elasticity than males
on chronically sun-exposed skin sites [21–23]. but the difference was not statistically significant.
This loss in elasticity is likely the major driver for Finally, Ma et al. [32] used the Cutometer MPA
visible facial skin wrinkling and sagging [24]. 580 to measure skin elasticity on the forehead
Skin elasticity is commonly measured using the and cheek of 240 healthy male and female volun-
non-invasive suction method [25–27]. The teers living in Shanghai, aged 20–70 years. There
Cutometer® is one of the more widely used was no significant difference in forehead skin
suction-­based skin elasticity instruments because elasticity between the genders. However, the
of its portability, speed and simplicity researchers did observe lower cheek skin elastic-
(Courage + Khazaka Electronic, Koln, Germany). ity (both R5 and R7) in older (age 50–70) males
The stress/strain curve can be divided into differ- than females. In summary, while skin elasticity
ent regions such as maximum deformation (Uf) declines with age in both males and females,
and immediate retraction (Ur). Ratios of these gender-­associated differences in skin elasticity at
absolute parameters yield relative parameters of any given age are small and likely not clinically
skin elasticity (e.g. Ur/Uf or R7) that are inde- meaningful.
pendent of skin thickness. Nedelec et al. [28]
used the Cutometer MPA 580 with a 6-mm probe
to measure skin elasticity at 16 body sites on 121 1.7 Facial Wrinkling
males and 120 females who were mostly Asian or
Caucasian and aged between 20 and 85 years old. When it comes to facial wrinkling, which sex
They found no consistent trend for gender differ- ages faster, men or women? Chung et al. [33]
ences in skin elasticity (R7) across age groups. assessed facial wrinkling on 236 men and 171
Cua et al. [29] also did not observe a significant women using standardized visual grading scales.
difference in skin elasticity between males and The results suggest that while the pattern of facial
females though their sample size was very small. wrinkling is similar between the sexes, women
Ishikawa et al. [30] compared skin elasticity on showed more severe wrinkles after adjusting for
men vs. women in a large subject sample on mul- age, sun exposure and smoking. Gender-­
tiple skin sites. Specifically, they used the dependent differences in facial wrinkling should
Cutometer SEM 474 to measure skin elasticity also consider facial location. In the perioral
on the forearm, hand, finger and chest of 96 males region (upper lip), women exhibit more and
and 95 females ages 9–87. Again, there was no deeper wrinkles than men [34]. However, on the
significant difference in skin elasticity between forehead, men show an earlier onset and more
males and females. Luebberding et al. [31] used severe wrinkling at every age than women [32].
the Cutometer MPA 580 to measure skin elastic- Hamer et al. [35] measured facial wrinkling using
ity on the cheek, neck and dorsum of the hand in digital imaging in 3831 Europeans (58% female)
150 males and 150 females ages 20–74. Skin aged 51–98. Men had higher wrinkle area than
elasticity (Ur/Uf) declined with age in both gen- women in the younger age groups (<75) but
ders, but was only slightly higher in women than women showed more wrinkles in the older age
in men. The authors noted that there was a more group (>75). Chien et al. [36] developed photo-
rapid decline in elasticity in women after 40 years graphic scales for perioral and crow’s feet wrin-
of age. Firooz et al. [4] also used the Cutometer kles that were gender specific meaning that there
6 R. R. Wickett and G. G. Hillebrand

was a scale for men and a scale for women. They sebaceous gland density. Sebaceous gland den-
used the grading scales to assess facial wrinkling sity was found to be significantly lower in the
on 71 men and 72 women, aged 21–91 years. All lateral canthus than in the forehead on both males
subjects were graded using both scales. and females. However, while the sebaceous gland
Interestingly, a participant’s score on the female-­ density was significantly lower in females than in
specific scale differed significantly from the males in both facial regions, there was no signifi-
male-specific scale score showing that it is cant gender-dependent difference in wrinkle
important to use gender-specific scales for the depth.
visual grading of facial wrinkling. The research- In a cross-sectional study of skin condition,
ers found that perioral wrinkling was more severe Hillebrand and colleagues measured facial wrin-
in women than men. For participants older than kling in the periorbital area (under eye and crow’s
45 years, there was even greater gender disparity. feet wrinkles) on 147 Caucasian males and 183
Tsukahara et al. measured facial wrinkling in 173 Caucasian females, aged 10–78. Regression anal-
Japanese men and women [37]. Men showed ysis showed that both gender and age to be sig-
increased forehead wrinkles compared with nificant (p < 0.05) factors in describing the
women at all ages. However, the difference in variance in wrinkle severity (Fig. 1.2a). However,
facial wrinkle severity tended to disappear in the when other factors are considered in the regres-
older age groups and there were no gender-­ sion analysis, like the subject’s body mass index,
related differences at any age for upper eyelid smoking history in pack years and years working
wrinkles. In related work, 3D analysis of skin outside, gender drops out as a significant factor
replicas found that the depth of eye wrinkles in suggesting that some of the variance initially
men showed an annual variation with more wrin- explained by gender can be explained by other
kles at the corner of the eye in the fall compared gender-associated confounding factors. We will
to the spring; no such annual variation was discuss confounding factors more later in the
observed in women [38]. The varying density of chapter. Figure 1.2b shows the data in Fig. 1.2a
sebaceous glands on the face may partly explain replotted as age group means for males and
the variation in facial wrinkling at different facial females. While females had higher wrinkles than
sites. Tamatsu et al. [39] looked at cadaver skin men in all age groups, none of the pairwise com-
specimens from females and males ranging in parisons between males and females in any given
age from the 20s to 90s at age of death. The found age group were significantly different (one-way
a negative correlation between wrinkle depth and ANOVA, Tukey Test).

Internet Download Manager Key - Crack Key For U a pdf creator crack full - Crack Key For U 0.16 b 0.08
Females
Ulead GIF Animator 5.0.5 Free Download with Crack 0.14 Females
Periorbital W rinkle Severity

Males
Periorbital W rinkle Severity

Males
(wrinkle area fraction)

0.12 0.06
(wrinkle area fraction)

Females
(r2=0.63)
0.10

0.08 0.04
0.06
Males
(r2=0.58)
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0.02

0.00
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0 20 40 60 80 100
10-19 20-29 30-39 40-49 50-59 60-69 70-79
Age Age Range

Fig. 1.2  Wrinkle severity in the periorbital region for eximioussoft banner maker pro crack - Free Activators sent best fit linear regression curves. (b) Age group
Caucasian females and males. (a) Scatter plot where each means ± standard error
point represents a subject’s wrinkle severity. Lines repre-
1  Effects of Gender on Skin Physiology and Biophysical Properties 7

1.8 Confounding Factors dition and most enroll only females. In a cross-­
sectional study of 4025 women ages 40–74,
The differences observed between male and Cosgrove et al. found that higher intakes of vita-
female skin may be ascribed to intrinsic factors min C and linoleic acid and lower intakes of fats
like hormones [40] and other genetically deter- and carbohydrates are associated with better
mined variables or extrinsic factors like differ- skin-aging appearance [48]. Higher intakes of
ences in smoking, diet, sun protection and skin vegetables, fruit, olive oil, and legumes may
care routines. Even differences in facial expres- cause less skin wrinkling and are protective
sion patterns may differ between the sexes and against actinic damage [49]. Iizaka et al. mea-
influence skin condition, especially facial wrin- sured nutritional status and habitual dietary
kling [41]. Below we discuss confounding fac- intact, stratum corneum hydration and xerosis in
tors that should be considered when designing 118 older (>65) Japanese subjects, mostly
and interpreting clinical data for men and women. females [50]. They concluded that a dietary pat-
tern characterized by higher vegetable and fruit
intake was associated with a better skin condi-
1.8.1 Smoking History tion. Since men’s daily intake of fruits and vege-
tables is less than that of women [51], dietary
Smoking has been shown to increase facial wrin- differences in the sample population should be
kling [34]. A report by Okada et al. involving considered in interpretation and analysis of clini-
identical twins underscores the risk of smoking cal results as well as in clinical design.
on appearance and health. They compared facial
wrinkling in identical twins and showed that a
5-year difference in smoking history can have a 1.8.3 Skin Care Habits and Practices
noticeable effect on skin aging [42]. Similar
observations were reported by Doshi et al. [43]. A person’s daily skin care routine will undoubt-
The exact mechanism for how smoking affects edly affect their skin condition. Regular use of
skin wrinkling is not understood but may involve moisturizers will improve skin barrier function,
changes in skin barrier function and associated skin hydration, and lessen the advancement of
changes in chronic skin dryness caused both by wrinkling [14, 41]. Those who regularly protect
smoking and exposure to second-hand smoke their skin from acute and chronic sun exposure
[44] which is associated with having more wrin- will slow the advancement of skin aging. Male
kles [41, 43, 44]. Since men are more likely to facial skin is largely influenced by beard groom-
smoke than women (Centers for Disease Control ing routines [52, 53]. In this regard, many of the
and Prevention [45], smoking needs to be consid- differences observed between male and female
ered as a confounding variable when comparing skin may be attributable to differences in skin
the skin condition of males to females. care habits and practices, especially differences
on the face [54].

1.8.2 Diet and Nutrition


1.8.4 Sun Exposure
Consuming an adequate amount of fruit and veg-
etables has been shown to reduce the risk of Sun exposure is well known to be a major cause
excess weight gain, type 2 diabetes, cardiovascu- of wrinkling, especially in facial skin [23, 55–
lar disease, and specific cancers [46, 47]. Pezdirc 57]. When discussing gender differences in facial
et al. [47] has recently reviewed the summation wrinkles the relative tendency for sun exposure
of evidence linking diet and skin health. The and the frequency of sunscreen application
majority of studies conducted in this space focus should be considered as regular sunscreen use
on the effect of dietary supplements on skin con- may provide some protection against the signs of
8 R. R. Wickett and G. G. Hillebrand

photoaging [58, 59]. Haluza et al. reported that 3. Ogoshi K. Optical measurement of sebum excre-
tion using opalescent film imprint. The Sebumeter.
Australian men are more likely to suffer sun
In: Handbook of non-invasive methods and the skin.
exposure and less likely to use sunscreen com- Boca Raton: Taylor and Francis; 2006. p. 841–6.
pared to their female counterparts [60]. This may 4. Firooz A, Sadr B, Babakoohi S, Sarraf-Yazdy M,
explain the earlier onset [35] and more severe Fanian F, Kazerouni-Timsar A, et al. Variation of bio-
physical parameters of the skin with age, gender, and
wrinkling seen in men on the forehead [37] but is
body region. Sci World J. 2012;2012:386936.
not consistent with the higher levels of perioral 5. Fluhr JW, Bankova L, Dikstein S. Skin surface pH:
wrinkles seen in women [36]. mechanism, measurement, importance. In: Serup J,
GBE J, Grove GL, editors. Handbook of non-invasive
methods and the skin. 2nd ed. Boco Raton: Taylor and
Francis; 2006. p. 411–20.
1.9 Summary 6. Zlotogorski A. Distribution of skin surface pH on the
forehead and cheek of adults. Arch Dermatol Res.
One of most important and difficult questions 1987;279(6):398–401.
7. Ehlers C, Ivens UI, Møller ML, Senderovitz T, Serup
whenever comparing measured properties
J. Females have lower skin surface pH than men. Skin
between two groups is whether statistically sig- Res Technol. 2001;7(2):90–4.
nificant differences are clinically relevant. We 8. Kim MK, Patel RA, Shinn AH, Choi SY, Byun HJ,
have reviewed and summarized many of the stud- Huh CH, et al. Evaluation of gender difference in skin
type and pH. J Dermatol Sci. 2006;41(2):153–6.
ies aimed at improving our understanding of the
9. Man MQ, Xin SJ, Song SP, Cho SY, Zhang XJ, Tu
similarities and differences between male and CX, et al. Variation of skin surface pH, sebum con-
female skin with particular attention to differ- tent and stratum corneum hydration with age and
ences in biophysical skin properties. We noted gender in a large Chinese population. Skin Pharmacol
Physiol. 2009;22(4):190–9.
that results depended on the method used, the
10. Nilsson GE. Measurement of water exchange through
body site being measured, the age of the subjects, the skin. Med Biol Eng Comput. 1977;15:209–18.
and their prior history of smoking, sun exposure, 11. Fluhr JW, Feingold KR, Elias PM. Transepidermal
and use of skin care products. The most consis- water loss reflects permeability barrier status: valida-
tion in human and rodent in vivo and ex vivo models.
tent difference between the genders reported in
Exp Dermatol. 2006;15(7):483–92.
this review is lower sebum production in women, 12. Chilcott RP, Farrar R. Biophysical measurements of
especially over the age of 50. However, because human forearm skin in vivo: effects of site, gender,
of the high individual variability in sebum output chirality and time. Skin Res Technol. 2000;6(2):64–9.
13. Wilhelm KP, Cua AB, Maibach HI. Skin aging. Effect
there is overlap between the high sebum produc-
on transepidermal water loss, stratum corneum hydra-
ing females and low sebum producing males tion, skin surface pH, and casual sebum content. Arch
(Table 1.1). Thus care must be taken when draw- Dermatol. 1991;127(12):1806–9.
ing conclusions from the differences reported in 14. Hadi H, Awadh AI, Hanif NM, Md Sidik NF, Mohd
Rani MR, Suhaimi MS. The investigation of the skin
the studies summarized here.
biophysical measurements focusing on daily activi-
ties, skin care habits, and gender differences. Skin Res
Acknowledgements The authors wish to thank Aimee Technol. 2016;22(2):247–54.
Herbel (Amway Corporation) for her help in collecting 15. Barel AO, Clarys P. Study of the stratum corneum
the pH data in Fig. 1.1. barrier function by transepidermal water loss mea-
surements: comparison between two commercial
instruments: Evaporimeter and Tewameter. Skin
Pharmacol. 1995;8(4):186–95.
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18. Berardesca E. EEMCO guidance for the assessment 33. Chung JH, Lee SH, Youn CS, Park BJ, Kim KH, Park
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1980;75(6):500–7. R, et al. Perioral wrinkles are associated with female
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10 R. R. Wickett and G. G. Hillebrand

49. Purba MB, Kouris-Blazos A, Wattanapenpaiboon


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Racial and Gender Influences
on Skin Disease 2
Daniel Callaghan and Neelam A. Vashi

2.1 Introduction 2.1.1 Physiologic Differences

Skin of color typically refers to individuals of 2.1.1.1 Skin Physiology


African, Afro-Caribbean, Asian, Hispanic, Skin is routinely characterized by the Fitzpatrick
Native American, Middle Eastern and Pacific scale, a classification scheme based on how one
Island backgrounds. In the United States, indi- reacts to sun exposure. Type I skin is fair, burns
viduals from these groups made up 38% of the easily and does not tan. Type VI skin is dark
population in 2014, which is expected to increase brown or black, tans and never burns. Although
to 56% by 2060 [1]. large variation exists within the SOC population
Due to differences in skin physiology as well (SOC), generally speaking, SOC is generally rep-
as to different cultural practices, there are several resented by Fitzpatrick types III–VI skin.
dermatologic conditions that affect these popula- The hallmark feature of skin of color is the
tions at a higher rate compared to Caucasians. amount and distribution of melanin. Darker skin
Furthermore, there are a number of diseases that phenotypes have larger, non-aggregating melano-
disproportionately affect males and females somes distributed throughout the epidermis.
within these populations. In this chapter, we will Conversely, fairer skinned individuals have
discuss categories of diseases that are more com- smaller, aggregated melanosomes which are not
monly seen in these ethnic groups, including fol- present in the upper layers of the epidermis [2].
licular, scarring, and pigmentary disorders with a Due to this increased melanin, Black skin trans-
special focus on their epidemiology and mits only 7.4% of ultraviolet (UV) radiation,
pathogenesis. compared to 29.4% in Caucasian skin [3]. While
this pigmentation offers protection against some
diseases seen more commonly in Caucasians,
such as non-melanoma skin cancer, it makes those
with darkly pigmented skin more susceptible to
other diseases, particularly pigmentary disorders.
D. Callaghan
Boston University Medical Center, Boston, MA, USA The stratum corneum in skin of color is more
e-mail: daniel.callaghan@bmc.org compact due to greater intercellular cohesion.
N. A. Vashi (*) Although there is no difference in dermal thick-
Dermatology, Boston University Center for Ethnic ness, Black skin has more numerous and larger
Skin, Boston University School of Medicine, fibroblasts, which is thought to partially explain
Boston, MA, USA why they are at an increased risk of keloid
e-mail: nvashi@bu.edu

© Springer International Publishing AG, part of Springer Nature 2018 11


E. Tur, H. I. Maibach (eds.), Gender and Dermatology,
https://doi.org/10.1007/978-3-319-72156-9_2
12 novabackup download - Crack Key For U D. Callaghan and N. A. Vashi

FabiFlter Pro Crack+ License And Keygen Key Free Download 2021. Additionally, Black skin has collagen 2.2  ollicular and Scarring


F
fibers that are smaller but more closely stacked Disorders
together. Of note, studies regarding physiologic
differences in eccrine, apocrine and sebaceous 2.2.1 C
 entral Centrifugal Cicatricial
glands in different races have demonstrated con- Alopecia
flicting results [2, 4].
2.2.1.1 Introduction
2.1.1.2 Hair Physiology Central centrifugal cicatricial alopecia (CCCA),
Individuals of African descent have hair that is formerly known as hot comb alopecia or follicu-
characterized by flat, elliptical strands with lar degeneration syndrome, is a disease seen
curved follicles, which leads to tightly spiraled almost exclusively in African American women,
hair. Blacks also have fewer elastic fibers anchor- characterized by scarring hair loss first seen on
ing hair follicles to the dermis. Conversely, Asian the vertex of the scalp.
hair is rounder, with the largest cross-sectional
area relative to other ethnicities, resulting in hair 2.2.1.2 Epidemiology
that is generally straighter [5, 6]. These variations CCCA is the most common scarring alopecia
account in part for the different clinical charac- filmora 9 crack - Free Activators among African American women and is rarely
teristics seen in the hair of these ethnic groups. reported in other ethnic groups. Large population
African Americans tend to have hair that is drier, based studies are lacking, but one study of African
slower growing and more fragile compared to American women in the Southeastern United
Caucasians. Conversely, Asian hair tends to be States found the incidence of CCCA to be 5.6%
thicker in diameter with faster growth [7, 8]. [9]. Although it is predominantly seen in women,
it has been reported in African American men [10].

2.1.2 Cultural Differences 2.2.1.3 Pathogenesis


CCCA is an inflammatory disorder which ulti-
Due to these physiologic differences, cultural dif- mately results in scarring; however, the specific
ferences exist in terms of how the SOC popula- reasons why this inflammation occurs remain
tion cares for their skin and hair. For example, elusive and are likely multifactorial.
African Americans may braid their hair in corn-
rows as a symbol of cultural identity and because Skin of Color
it offers a lower maintenance hairstyle. Hair Despite the fact that the specific pathogenesis of
extensions and weaves are used to give the hair a CCCA is unclear, one prevailing theory is that it
longer, straighter or more voluminous appear- is due in part to traumatic hair styling practices,
ance. Given the curly nature of Black hair, it is which are much more common in Blacks. These
also common for them to straighten their hair include tight braids, weaves, or cornrows and the
with chemicals or heat such as hot combs, flat use of chemical relaxers, texturizers, and/or heat.
irons and blow dryers. Alternatively, Sikh men Although this theory has been reinforced by stud-
and women do not cut their hair but rather allow ies in which a significant association between
it to grow as a symbol of devotion to God. They CCCA and hairstyling practices was observed,
also wear turbans to care for their hair and as a other studies were unable to find a similar asso-
sign of identity and equality. Over time, many of ciation [9, 11].
these hair styling practices can lead to irritation It has also been suggested that there is a
and follicular damage which propagates the genetic component to the development of CCCA,
inflammatory cascade. Ultimately, these different as it has been described to run in families. Dlova
physiologic and cultural differences have been et al. observed 14 South African families in
implicated in the pathogenesis of several diseases which an autosomal dominant pattern of CCCA
seen more commonly in skin of color. was demonstrated. Furthermore, 20% of these
2  Racial and Gender Influences on Skin Disease 13

individuals reported no history of traumatic hair- be started as soon as possible. It is important to


styling, which suggests that there is more to the discuss and set expectations with the patient,
pathogenesis of CCCA than these practices, and a including the fact that it is challenging to predict
genetic component may also be at play [12]. the course of the disease. Furthermore, if scarring
has already occurred, it is important to make the
Gender patient aware that regrowth will be quite limited.
Males rarely use the hair styling practices which Unless these expectations are outlined early and
have been implicated in the pathogenesis of CCCA, clearly, at future visits, patients may be frustrated
which may explain why it is far less common for with their management.
them to be affected. However, the fact that it has Given the implication of certain hair styling
been seen in males, particular African American XMedia Recode 3.4.7.0 Crack Serial Key - Crack Key For U techniques in the pathogenesis of CCCA, it
males, supports the claim that there may be an should be stressed to patients to avoid such prac-
underlying genetic component to the disease [10]. tices, even if they have denied using them in the
past. Being a disease of inflammation, topical or
2.2.1.4 Clinical Features intralesional steroids are typically used. Oral tet-
As the name suggests, CCCA generally begins on racyclines have also been used in the treatment of
the crown or vertex of the scalp, and slowly CCCA. Other therapies that have been reported
expands centrifugally. In early stages, mild hair anecdotally include antimalarials, topical calci-
thinning may make the disease difficult to distin- neurin inhibitors, minoxidil, thalidomide, cyclo-
guish from androgenetic alopecia. Although it Transparent Taskbar 2020.2 Free Download sporine and mycophenolate mofetil [13].
typically expands slowly, it can eventually prog- Patients may present to clinic specifically
ress centrifugally to affect the entire crown of the inquiring about the effectiveness of hair trans-
scalp. Left untreated, scarring occurs and the scalp plantation, and in some cases may have already
becomes smooth and shiny, with follicular dropout consulted with a hair transplant surgeon.
and preservation of a few short, brittle hairs [13]. Although hair transplantation has been reported
Patients may complain of mild pruritus or ten- to be successful in patient who have had stable
derness in the area that is affected, which can be disease for at least 9–12 months, patients should
a sign of disease activity. In certain cases, patients be educated on the potential need for multiple
may present with superimposed folliculitis decal- hair transplant sessions, the need for continued
vans, with pustules and crusting. medical therapy, and the possibility of disease
recurrence [15].
2.2.1.5 Histology
Depending on the stage of the disease, CCCA
demonstrates a follicular lichenoid lymphocytic 2.2.2 Traction Alopecia
infiltrate when caught early, which leads to fol-
licular fibrosis as it progresses. Features that help 2.2.2.1 Introduction
make the diagnosis include follicular miniatur- Traction alopecia (TA) is another form of scar-
ization, premature desquamation of the inner root ring alopecia that is most prominently seen in
sheath, focal preservation of sebaceous glands, women of color. It develops in the setting of hair
naked hair shafts, compound follicular structures, styling techniques that create prolonged tension
perifollicular fibrosis and/or inflammation, and or repetitive pulling on hair.
lamellar hyperkeratosis and parakeratosis camtasia studio 5 - Crack Key For U the
hair canal [14]. 2.2.2.2 Epidemiology
TA is almost exclusively reported in women and
2.2.1.6 Treatment is most frequently seen in African Americans.
There are limited treatment options available for That said, it has also been described in other eth-
CCCA, and results are often unsatisfactory. As it nic groups, and the prevalence rate has also been
can ultimately lead to scarring, treatment should reported to be relatively high in Hispanics [16].
14 D. Callaghan and N. A. Vashi

Although it is far less commonly described in Although clinical history is crucial in making
males, they can also be affected; for example, TA this diagnosis, it is not uncommon for patients to
has been reported among Sikh males who wear deny styling their hair in a manner that predis-
their hair twisted tightly under turbans [17]. One poses them to TA. When the history does not sup-
study looking at 874 South African adults found port the diagnosis, the clinician may look for the
that 31.7% of women had TA compared with just fringe sign to help identify the disease. The
2.2% of men [18]. ‘fringe sign’ describes the presence of short
retained hairs along the hairline and can help dis-
2.2.2.3 Pathogenesis tinguish TA from other forms of hair loss such as
Traction alopecia develops when hairstyling ophiasis alopecia areata. It has been reported in
practices cause tension on the hair follicle, which up to 100% of women with TA affecting the fron-
over time leads to inflammation, fibrosis and per- tal or temporal hairlines [16].
manent alopecia.
2.2.2.5 Histology
Skin of Color Histologically, early TA demonstrates decreased
The increased prevalence of TA in Blacks is follicular number but preservation of the seba-
explained both by filmora 9 crack download - Free Activators and physiologic differ- ceous glands. Features of trichomalacia, includ-
ences. As described before, Black hair grows in a ing twisting or deformation of anagen bulbs can
tight spiral pattern, making it more susceptible to also be seen when caught early. Depending on the
breakage when manipulated. Furthermore, stage, follicular scarring may or may not be pres-
Blacks more commonly use hair styling tech- ent. As the disease progresses, the number of
niques such as braids, weaves, chemical relaxers sebaceous glands may be reduced and hair folli-
and heat, which puts more tension on their hair cles become surrounded by a lymphocytic infil-
and increases their risk of developing TA. For trate and fibrosis [20]. However, these findings
instance, it has been shown that chemically pro- are not pathognomonic and clinicopathologic
cessed hair has a greater risk of developing TA correlation is necessary to make an accurate
[19]. TA can also be seen in Hispanics who wear diagnosis.
their hair in tight ponytails. Japanese women
have also been reported to get TA on the occipital 2.2.2.6 Treatment
or temporal scalp from wearing their hair in a The first step in the treatment of TA is cessation
tight bun [16]. of any hairstyling technique which may be con-
tributing to the disease process. It may be diffi-
Gender cult to convince patients to change their
The increased prevalence in women is explained hairstyling practices, which they have often been
by the fact that they are far more likely to style using for years. As the hair styling practices that
their hair using the aforementioned practices. lead to TA are often started in childhood, it is
important to also educate parents about this risk
2.2.2.4 Clinical Features to help prevent the disease.
TA is most commonly seen in the frontal and In the setting of active inflammation, topical
temporal region of the scalp but can present or intralesional steroids can be used. Intralesional
anywhere depending on the hair styling prac- administration of steroids should be performed at
tice. When caught early, there may be perifol- the periphery of the hair line to prevent retained
licular erythema, papules or pustules. In a study hair from being lost. Oral antibiotics are also uti-
involving 41 patients with TA, including 12 lized in cases of TA when there is clinically
Hispanic patients, Samrao et al. reported clini- apparent inflammation. With patients who have
cally evident inflammation in 54% of African lost hair as a result of TA but have not yet devel-
American women compared with 17% of oped scarring, topical minoxidil may be benefi-
Hispanic women [16]. cial [21].
2  Racial and Gender Influences on Skin Disease 15

As with other scarring alopecias that are diffi- intrafollicular canal or sebaceous glands.
cult to manage medically, camouflage techniques Antigens that have been implicated include nor-
can be effective and can help improve patients’ how to use charles proxy mal skin flora, demodex, desquamated keratino-
quality of life. Surgical options, including follic- cytes, sebum and cosmetics [27, 28]. This
ular unit transplantation and mini- or micrograft- inflammation results in damage to the hair shaft,
ing have also been reported to be effective in the with the resulting clinical changes described in
appropriately selected patient [22]. AKN. Other reported etiologic factors have
included seborrheic dermatitis, Staphylococcus
aureus infection, and elevated serum testosterone
2.2.3 Acne Keloidalis Nuchae levels [29].

2.2.3.1 Introduction Skin of Color


Acne keloidalis nuchae (AKN) is a form of Previously, AKN was thought to be the result of
chronic folliculitis most frequently seen in Black inward growth of hair leading to a foreign body
males. It is characterized by papules and pustules reaction and subsequent inflammation. The spi-
on the occipital scalp and posterior neck, which raled nature of hair in Blacks would make them
over time can develop into keloid-like plaques more susceptible and explains why they are more
and scarring alopecia. commonly affected by the disease. That being
said, there is no clinical or histologic evidence to
2.2.3.2 Epidemiology substantiate this claim. For instance, one South
AKN has been described in all races but is most African study did not find an association between
frequently seen in Black men after adolescence the prevalence of AKN and the use of clippers as
and under the age of 55. In decreasing incidence opposed to razors [18]. Furthermore, one author
it also affects Hispanic, Asian and Caucasian observed that ingrown hairs are not commonly
males [23]. Knable et al. studied 453 male foot- seen in AKN as they are in PFB [27, 30].
ball players between the ages of 14 and 27, and If this theory is to be disregarded, it is unclear
found that while AKN was seen in 24% of black why there is an increased prevalence of AKN in
players, no white players were affected [24]. Blacks. If one subscribes to the thought that AKN
Although 20 times more bs player pro apk - Activators Patch in men, women is a primary cicatricial alopecia resulting from
can also be affected by it [25]. immune dysregulation, it may be that there is a
genetic component which predisposes these indi-
2.2.3.3 Pathogenesis viduals to the disease.
Despite its name, AKN is not a variant of acne
vulgaris, and the name folliculitis keloidalis Gender
nuchae has been suggested. The exact etiology is Similarly, our lack of understanding of the patho-
unknown, but it is a result of chronic inflamma- genesis of AKN makes it difficult to explain why
tion which ultimately leads to scarring and it is almost exclusively seen in males. However,
keloid-like plaques. that observation alone, coupled with the fact that
The development of AKN is typically attrib- it is rare before puberty or after the age of 55, has
uted to chronic trauma to the follicular scalp. led some to propose that there is a hormonal
Most investigators believe that AKN is a result of component involved. An increase in androgen
mechanical injury from friction and hair styling levels, androgen receptor sensitivity or increased
practices, such as the use of electric razors and activity of sebaceous glands may play a role [30].
shaving, which leads to irritation, occlusion,
trauma and inflammation [26]. 2.2.3.4 Clinical Features
Some propose that AKN is a primary cicatri- AKN initially presents as inflammatory papules
cial alopecia resulting from an immune response on the nape of the neck and posterior scalp, which
against antigens on the follicular epithelium, over time result in fibrosis and keloid-like
16 D. Callaghan and N. A. Vashi

plaques. These patients can also develop second- treatment option; however, the risk of scarring is
ary infection with pustules, subcutaneous an obvious concern. Unfortunately, the risk of at
abscesses and sinus drainage. Repeated inflam- least mild recurrence is nearly 50%, typically
mation leads to the destruction of hair follicles, within weeks to months of medication discontin-
fibrosis and ultimately scarring alopecia. uation [26].
Furthermore, the keloid-like plaques that develop
are usually devoid of hair.
These changes can be a significant cosmetic 2.2.4 Pseudofolliculitis Barbae
concern to patients and negatively affects their
quality of life [23, 31]. Similar to other inflam- 2.2.4.1 Introduction
matory disorders, these patients also complain of Pseudofolliculitis barbae (PFB) is a chronic, non-­
pruritus, and the lesions can be painful and tender infectious, inflammatory follicular disorder
to palpation. which results in erythematous papules most fre-
quently found in the beard area. Given the simi-
2.2.3.5 Histology larities in appearance of AKN and PFB, the two
Histologic characteristics of AKN include peri- diseases were previously thought to be on the
follicular, lymphocytic and plasmacytic inflam- same spectrum, with the difference being the
mation most intense at the level of the isthmus location they affected. However, the two diseases
and lower infundibulum, lamellar fibrosis, loss of are now thought to be separate entities, each with
sebaceous glands, thinning of the follicular epi- a different pathogenesis.
thelium and total epithelial destruction with
residual “naked” hair fragments [28]. These his- 2.2.4.2 Epidemiology
tologic findings closely resemble other forms of PFB is most often found in Black males, with the
cicatricial alopecia, which is what has led some reported incidence varying from 45% to 83%. It
to propose it to be a form of primary cicatricial is also seen in other populations who may have
alopecia. Vit Registry Fix Pro 12.6.6 Free Download with Crack Vit Registry Fix Pro 12.6.6 Free Download with Crack more tightly curled hair, including Hispanics and
simplesoft simple invoice crack Middle Easterners. It is less commonly observed
2.2.3.6 Treatment in women [32].
Early treatment correlates with a good prognosis;
however, as the disease progresses, it can be more 2.2.4.3 Pathogenesis
difficult to treat and more invasive measures must PFB occurs because of ingrown hairs, which
be utilized. induce a foreign body inflammatory reaction
Management is typically first directed at upon re-entering the skin through extrafollicular
avoiding any inciting factors that may be causing or transfollicular penetration. Certain hair styling
irritation. Mild disease can be managed medi- techniques, such as pulling the skin taut while
cally with topical or intralesional steroids, topical shaving and/or cutting the tip to a sharp point,
or oral antibiotics, particularly tetracyclines, and can make re-entry more likely.
retinoids [26].
Light and laser therapies, including the 1064-­ Skin of Color
nm neodymium-doped yttrium aluminum garnet Blacks have tightly spiraled hairs, which curve in
(Nd:Yag) laser and targeted UVB light, have such a manner to emerge almost parallel to the
offered promising results with mild side effects skin. Rather than continue to grow outward, this
including transient erythema and mild burning. orientation puts them at risk to curl and re-enter
These treatment options work to destroy the hair the skin. Beyond this, some individuals may have
follicle and decrease the inflammation implicated a genetic predisposition to developing PFB, which
in the pathogenesis of the disease. was demonstrated by Winter et al. who found that
Surgical or cryosurgical treatment with sec- a defect in a hair follicle keratin increased the risk
ondary intention healing may be an effective of developing PFB by a factor of 6.12 [33].
2  Racial and Gender Influences on Skin Disease 17

Gender electric shavers. However, that can be an incon-


PFB is thought to affect males more so than venience for individuals who prefer to be closely
females because of its close association with speedify vpn reviews shaved, and is impractical for others who may be
shaving. That being said, women can also develop required to be closely shaved. For those who are
PFB. One study found that hormonal disorders able to stop shaving, remission is often seen
leading to hyperandrogenism and hirsutism is a within 30 days [36].
risk factor for women to develop PFB [34]. For men who are unable or unwilling to avoid
shaving, shaving techniques that have been pro-
2.2.4.4 Clinical Features superantispyware registration code 2021 posed to help reduce the burden of PFB include
PFB presents as firm, follicular or perifollicular shaving regularly to prevent hair from growing
papules most often found on the neck and cheeks long enough to re-enter the skin, preparing the
in men. Some papules may contain visible hairs. skin beforehand with warm water and a gentle
When it does affect women, the chin is the most cleanser to soften the hair, applying shaving foam
commonly area affected, especially in hirsute or gel to provide a protective anti-friction layer,
women who shave or pluck unwanted hairs. keeping the skin relaxed rather than pulling taut,
Although it is associated with shaving in men, it and using a technologically advanced multiblade
should be noted that the mustache and nuchal razor or foil-guarded manual single-blade razor.
areas are rarely affected [32, 35]. The use of after-shave products containing mois-
Although secondary infection can occur, pus- turizing ingredients also help rehydrate and com-
tules are rare in PFB, which can help distinguish fort the skin [35].
it from acne vulgaris. No comedonal lesions are For PFB that cannot be controlled by non-­
seen in PFB, which also helps distinguish it from medical interventions, retinoids have been
acne. reported to improve the disease, with the thought
PFB must also be distinguished from trau- that they relieve hyperkeratosis and remove the
matic folliculitis, more commonly known as thin covering of epidermis that the hair becomes
razor burn. Traumatic folliculitis occurs when embedded in when re-entering the skin. Mild
shaving is performed too closely. It presents as topical corticosteroids can also be used temporar-
painful follicular papules which may be confused ily to reduce inflammation [32]. In addition, topi-
for PFB but disappear within 24–48 h. PFB, con- cal eflornithine hydrochloride cream can be used
versely, persists for weeks after cessation of to slow hair growth.
shaving. For severe disease, especially in the setting of
PFB may be associated with pruritus and pain frequent superinfection with the development of
and may be complicated by postinflammatory pustules and abscess formation, topical or oral
hyperpigmentation (PIH), scarring, and forma- antibiotics may be indicated, with tetracyclines
tion of keloids [32]. commonly employed [35]. Laser therapy has
been used successfully, with the Nd:YAG
2.2.4.5 Histology 1064 nm lasers having the best safety and effi-
Histopathologically, PFB is characterized by a cacy profile for use in SOC patients.
foreign body inflammatory response to hair re-­
entering the skin. Epidermal penetration shows
invagination with an inflammatory infiltrate, 2.2.5 Dissecting Cellulitis
which becomes more intense as the hair reaches
the dermis [21]. 2.2.5.1 I ntroduction
Dissecting cellulitis of the scalp (DCS) is a form
2.2.4.6 Treatment of primary neutrophilic cicatricial alopecia. It is a
Given its pathogenesis, the first recommendation chronic inflammatory disorder resulting in scar-
in the management of PFB is often cessation of ring alopecia more frequently seen in Black
shaving, the only curative treatment, or use of males. It makes up a component of the follicular
18 D. Callaghan and N. A. Vashi

occlusion tetrad, which also includes hidradenitis erature, it suggests that there is a genetic risk fac-
suppurativa (HS), acne conglobata, and pilonidal tor, which may be predisposing Black patients to
cysts. the disease disproportionately [40].

2.2.5.2 Epidemiology Gender


DCS is most commonly seen in Black males It is also unclear why males are affected more pre-
between their third to fifth decades of life, with dominantly than females. Hormones have been
only 10% of cases involving Caucasians [37]. suggested to play a role in its pathogenesis, and
Although it can affect women, it is rare. A retro- one retrospective review found that 3/21 (14%) of
spective study of 51 patients with DCS in France patients associated the onset of their disease with
found that 65% were skin type IV or above, and use of anabolic-androgenic steroids [41].
only 1 was female [38]. One third of patients with
DCS have coexisting acne conglobata or hidrad- 2.2.5.4 Clinical Features
enitis suppurativa, and are thought to be at an Dissecting cellulitis typically begins as a follicu-
increased risk for developing HLA-B27 negative lar pustule on the occipital or vertex of the scalp.
spondyloarthropathy [21]. Patients may develop multiple pustules which
can evolve into nodules and abscesses that form
2.2.5.3 Pathogenesis interconnecting sinus tracts. Over time, if
The overlying pathogenesis of DCS is thought to untreated, the scalp takes on a cerebriform, boggy
be the result of a defect in follicular keratiniza- appearance with resulting overlying scarring alo-
tion, which leads to occlusion of the piloseba- pecia. This can be further complicated by hyper-
ceous unit and accumulation of sebaceous and trophic scarring and keloids. Patients’ quality of
keratinous material. This leads to subsequent fol- life can be severely affected as the lesions can be
licular expansion and inflammation. Dilated fol- both painful and disfiguring [4, 37, 39].
licles can rupture, further propagating the
inflammation with a neutrophilic and granuloma- 2.2.5.5 Histology
tous response. Secondary infection can occur Similar to other inflammatory, scarring diseases,
with the development of folliculitis. Ultimately, the histopathologic features of DCS demonstrate
chronic inflammation results in nodules and great variability based on the stage of the disease
abscesses which can form interconnecting sinus examined. In early lesions, dilatation of the
tracts and can also result in scarring and alopecia. infundibula is observed, with a surrounding peri-
These sinus tracts can serve as niduses for bacte- follicular, mixed, neutrophilic and lymphoplas-
rial overgrowth and inflammation, resulting in a macytic infiltrate, particularly affecting the lower
cyclical inflammatory and scarring process that portion of the infundibula. As the disease pro-
can be difficult to control [21, 39]. gresses, deep-seated abscesses in the adventitial
The inciting factor for this process has yet to dermis and subcutis form and follicular destruc-
be fully elucidated. One theory that has been pro- tion results, with eventual fibrosis. Sinus tracts
posed is it is the result of loss of immune toler- can be seen which are lined with squamous epi-
ance to alloantigens in the hair follicle, which thelium [42].
leads to the inflammatory response seen [38].
2.2.5.6 Treatment
Skin of Color Management of DSC remains challenging.
It is unclear why DCS is seen more frequently in Therapy is initially managed medically, with top-
Blacks. The role of hair type and hair styling ical or intralesional steroids, antibacterial cleans-
practices has also been suggested to be impli- ers, topical or oral antibiotics, prednisone and
cated in the pathogenesis of DCS; however, isotretinoin as monotherapy or in combination
strong evidence supporting this is sparse. As with rifampin. Although relapse is common after
there have been cases of familial DCS in the lit- discontinuation, there are some reports of isotret-
2  Racial and Gender Influences on Skin Disease 19

inoin causing a sustained remission for up to 0.034% of the Asian population is affected by
2.5 years [43]. TNF-α inhibitors, which have nevus of Ota, and it is five times more likely to be
been used to treat HS and acne conglobata, have seen in women than men [47, 48]. They have
been reported to show improvement in some been reported to be unilateral in 90% of cases and
patients with refractory DSC; however, not all bilateral in 5–10% of cases [48]. Dermal melano-
patients show a response [44, 45]. cytoses can be congenital or acquired. Nevus of
Resistant DCS has been successfully treated Ota is typically congenital; however, may appear
with laser therapy, including an 800 nm pulsed during puberty. When small lesions are acquired,
diode laser and the 1064 nm long-pulse Nd:YAG they are called Sun’s nevus if unilateral, and
laser [21]. Hori’s nevus if bilateral. A population-based
Though medical options can be valuable in sta- study in Taiwan described the overall incidence
bilizing the disease process, some feel they can of ABNOM to be 0.8% [46].
never offer a sustainable response as they are
unable to address the existing sinus tracts, which 2.3.1.3 Pathogenesis
serve as a nidus for infection, drainage, and con- Nevus of Ota is thought to be the result of migration
tinued inflammation. For this reason, severe dis- arrest of melanocytes on their way from the neural
ease has been treated with complete scalp excision crest to the epidermis [49]. It has been hypothesized
followed by split-thickness skin grafting, although that the acquired variant of these lesions may be
side effects and recurrence have been reported to related to reactivation of existing dermal melano-
occur. More recently, Powers et al. reported ben- cytes which were previously misplaced during
efit from a staged excision, which provides the embryological development [50]. One recent
benefits of more targeted focus of disease control review of 102 patients found sun exposure (47.1%),
and preservation of hair-­bearing portions of the pregnancy (32.0%), cosmetics (29.4%), sensitive
scalp, leading to better outcomes [37, 39]. skin (22.6%) and positive family histories (21.6%)
to be highly related to the development of ABNOM
[51]. Given the higher prevalence among Asians, a
2.3 Disorders of Pigmentation genetic component likely exists. It has also been
suggested that hormones play a role in the patho-
2.3.1 Nevus of Ota genesis as pregnancy has been associated with the
development of ABNOM.
2.3.1.1 Introduction
Dermal melanocytoses comprise a group of 2.3.1.4 Clinical Features
melanocytic lesions which can be congenital or Nevus of Ota presents as a bluish or gray-brown
acquired. Nevus of Ota, acquired bilateral nevus discoloration in areas innervated by the first two
of Ota-like macules (ABNOM, also known as branches of the trigeminal nerve. Roughly two-­
Hori’s nevus) and acquired unilateral nevus of thirds of patients will have characteristic involve-
Ota-like macules (also known as Sun’s nevi) are ment of the ipsilateral sclera.
three facial dermal melanocytoses which are far ABNOM present as blue-brown and/or slate-­
more commonly found in Asian females. gray macules occurring in a speckled pattern
Controversy exists as to whether or not these bilaterally on the malar regions, and can also
lesions belong on a spectrum or are clinically involve the forehead, upper eyelids, cheeks and
separate entities [46]. Histology and treatment of nose [46]. Although some consider these lesions
all lesions are similar. to be on the same spectrum of Nevus of Ota, oth-
ers distinguish them by their adult onset, speck-
2.3.1.2 Epidemiology led and bilateral pattern, and lack of mucosal
Nevus of Ota primarily affects Asian populations involvement [52].
but can also be seen in Africans and Indians. It is Patients with nevus of Ota are at increased risk
rarely seen in Caucasian patients. Approximately for glaucoma, and therefore should Vit Registry Fix Pro 12.6.6 Free Download with Crack followed
20 D. Callaghan and N. A. Vashi

with routine eye exams [53]. Malignant transfor- a complex interplay of genetics, hormones, and
mation of dermal melanocytoses is rare. A recent exposure to ultraviolet and visible light.
review found a total of 14 cases of cutaneous
melanoma arising in dermal melanocytoses, with 2.3.2.2 Epidemiology
10 of those arising within nevi of Ota, and 4 aris- The prevalence of melasma varies widely based
ing within nevi of Ito. Interestingly, of the 10 on the ethnic and geographic composition of the
reported cases of cutaneous melanoma arising in population. When populations of skin of color
association with nevus of Ota, 8 of the patients have been studied, the prevalence of melasma has
were Caucasian, with the race/ethnicity of the ranged from 8.8% to 41% [57]. Most studies
two additional patients not being reported [54]. report the incidence of melasma being highest in
Although asymptomatic, as nevus of Ota can be skin types III–V. It predominantly affects women,
cosmetically disfiguring, patients can suffer from with one population based study out of Brazil
severe emotional or psychological distress [47]. reporting it in 6% of men [58].

2.3.1.5 Histology 2.3.2.3 Pathogenesis


Lesions microsoft office crack 2010 - Crack Key For U irregularly shaped melano- Pathophysiology remains unclear. Ultraviolet
cytes dispersed throughout the dermis. and visible light exposure, pregnancy, sex hor-
mones, use of oral contraceptives, steroids,
2.3.1.6 Treatment inflammation and photosensitizing drugs are
As with other pigmentary disorders, photoprotec- known triggers that have been implicated in its
tion is a cornerstone of therapy. Cosmetic camou- pathogenesis. In addition, melanocytes associ-
flage may also be utilized to help reduce the ated with melasma lesions are more biologically
burden of disease. Laser therapy is the treatment active when compared to normal skin; this is evi-
of choice for nevus of Ota. Traditionally denced by increased mitochondria, Golgi com-
Q-switched (QS) lasers, including the 694 nm QS plex, and rough endoplasmic reticulum [59]. The
ruby, 755 nm QS alexandrite, and both the 532 growing knowledge on melasma pathogenesis
and 1064 nm QS Nd:YAG lasers showed the suggests a complex cellular interplay involving
most favorable clearance rates with the fewest melanocytes, keratinocytes, dermal fibroblasts,
side effects [47]. increased vascularity and increased mast cells.
More recently, picosecond lasers have been
shown to be safe and effective in the treatment of Skin of Color
these lesions [55]. Although not all lesions Although melasma is found in all ethnic groups,
respond to treatment, but for those that do studies have shown a higher prevalence in more
respond, recurrence rate after treatment is rare pigmented populations including Hispanic,
(0.8–2.1%) [56]. When the appropriate patient Japanese, Korean, Chinese, Indian, Pakistani,
and laser are selected, side effects are infrequent; Middle Eastern, and Mediterranean-African indi-
however, risk of post-inflammatory hyperpig- viduals [60, 61]. It may also be seen more in
mentation should always be considered in the these populations because of a genetic influence,
SOC population. which has been theorized based on its tendency
to run in families, with over 40% of patients
reporting having relatives affected with the dis-
2.3.2 Melasma ease [57].

2.3.2.1 Introduction Gender


Melasma is a common disorder of hyperpigmen- There is a clear association between hormones
tation with higher prevalence in females along and the development of melasma as it is most
with Fitzpatrick skin types III–IV and/or those of commonly seen among women and with the use
Hispanic descent. It is thought to be the result of of oral contraceptives and during pregnancy.
2  Racial and Gender Influences on Skin Disease 21

Despite this strong association, the specific role of melasma after beginning oral contraceptives,
hormones play in its pathogenesis is poorly they should be stopped if possible [52]. Topical
understood. However, it is known that human agents including hydroquinone, retinoids and
melanocytes have estrogen and progesterone azelaic acid have been reported with good suc-
receptors, and the expression of estrogen recep- cess in the treatment of melasma. Combination
tors appears to be increased in skin affected by creams have been shown to be more successful
melasma [62, 63]. than monotherapy [66].
Chemical peels may be useful for patients
2.3.2.4 Clinical Features with moderate to severe melasma that is magic dvd copier registration code presents as hyperpigmented macules tant to topical therapy. Superficial peels, includ-
coalescing into irregularly shaped patches most ing glycolic acid and salicylic acid peels, have
commonly found on the cheeks, upper lip, fore- been shown to be effective with few adverse
head, nose, cheek and chin. Extra-facial disease effects [67].
on sun-exposed areas can also occur. Under der- Laser and light based therapies, including
moscopy, when limited to the stratum corneum intense pulsed light, QS Nd:YAG and pulse dye
melasma presents as a well-defined brown to lasers, have been shown to be effective in severe
dark brown network. When it involves the lower or refractory disease. These therapies are limited
epidermis, it appears as lighter shades of brown by the fact that they demonstrate a high relapse
with a more irregular network. When there is also rate and carry the risk of side effects including
involvement of the dermis, it demonstrates a blue PIH, particularly in darker skin types [66]. Newer
or bluish-gray color [57]. lasers, such as those using picosecond technol-
Melasma can cause a significant amount of ogy, show promising results and limited side
psychological stress in patients and negatively effects.
affects their quality of life [64]. Oral agents have been used for the treatment
of melasma, with oral tranexamic acid showing
2.3.2.5 Histology the most promising results [68, 69]. Other agents
Melasma is characterized by hypertrophic mela- with a good safety profile that may have efficacy
nocytes and an increased amount of melanin seen include Polypodium leucotomos extract, carot-
in all layers of the epidermis along with a possi- enoid, melatonin and procyanidin. However,
ble increased number of melanophages. An these agents are most commonly used as supple-
increased number of melanocytes are not ments to other treatments options and are rarely
observed [59]. considered to be effective as monotherapy.

2.3.2.6 Treatment Conclusion


There are a wide variety of treatment options for Differences in cultural practices, particularly
melasma, and while many patients respond favor- hair styling practices, as well as physiologic dif-
ably, it can be resistant to treatment in others. ferences, such as an increased amount of mela-
Treatment is aimed at reducing the amount of nin, are implicated in many of the dermatologic
epidermal melanin and blocking solar radiation. conditions that are more commonly seen in skin
Melasma that is seen more intensely under of color. Similarly, differences in hair styling
Wood’s lamp examination typically responds practices between men and women, as well as
better to topical treatments [57]. differences in hormone levels, may explain why
The mainstay of treatment for melasma is pre- there is a discrepancy in the incidence of some
ventative therapy, including strict photoprotec- diseases in different genders. More research
tion with sunscreen and sun avoidance. This is must be performed to further illustrate the
especially valuable to reinforce in this patient pathogenesis behind these conditions, which
population, that may not be accustomed to wear- will allow for more targeted and effective treat-
ing sunscreen [65]. In women who note the onset ment options. Skin of color represents an incred-
22 D. Callaghan and N. A. Vashi

ibly heterogeneous group of individuals, and J Am Acad Dermatol. 2014;70(4):679–82. https://doi.


care must be taken to avoid making generaliza- org/10.1016/j.jaad.2013.11.035.
13. Herskovitz I, Miteva M. Central centrifugal cicatri-
tions about patients, but rather each patient must cial alopecia: challenges and solutions. Clin Cosmet
be treated individually for optimal results. Investig Dermatol. 2016;9:175–81.
14. Miteva M, Tosti A. Dermatoscopic features of cen-
tral centrifugal cicatricial alopecia. J Am Acad
Vit Registry Fix Pro 12.6.6 Free Download with Crack Dermatol. 2014;71(3):443–9. https://doi.org/10.1016/j.
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Bernárdez C, Molina-Ruiz AM, Requena
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Arch Dermatol. 2016;136(4):479–84. https://doi. alopecias. Actas Dermosifiliogr. Aomei Backupper Crack org/10.1001/archderm.136.4.479. https://doi.org/10.1016/j.ad.2014.07.006.
29. Lee A, Cho S, Yam T, Harris K, Ardern-Jones
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M. Staphylococcus aureus and chronic folliculocen- of the scalp: response to isotretinoin. Br J Dermatol.
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J Dermatol. 2016;175(2):410–3. 44. Mansouri Y, Martin-Clavijo A, Newsome P, Kaur

30. Ogunbiyi A. Acne keloidalis nuchae: prevalence,
MR. Dissecting cellulitis of the scalp treated with
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Investig Dermatol. 2016;14(9):483–9. two agents. Br J Dermatol. 2016;174(4):916–8.
31. Salami T, Omeife H, Samuel S. Prevalence of acne https://doi.org/10.1111/bjd.14269.
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movavi photo editor activation key 2007;46(5):482–4. https://doi.org/10.1111/j.1365-4632. inhibitors in netbalancer 9.12.6 crack - Free Activators dermatological university department:
2007.03069.x. retrospective evaluation of 118 patients. Dermatol
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lis nuchae and pseudofolliculitis barbae: are preven- ashampoo photo commander 16 crack download - Crack Key For U dth.12222.
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35. Gray J, McMichael AJ. Pseudofolliculitis barbae:
50. Hori Y, Kawashima M, Oohara K, Kukita A. Acquired,
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36. Conte M, Lawrence J. Pseudofolliculitis barbae. No triggering factors for acquired, bilateral nevus of Ota-­
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38. Badaoui A, Reygagne P, Cavelier-Balloy B, et al. N. Glaucoma in oculodermal melanocytosis.
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Br J Dermatol. 2016;174(2):421–3. https://doi. arising in a nevus of Ito: novel genetic mutations
org/10.1111/bjd.13999. and a review of the literature on cutaneous malignant
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40. Bjellerup M, Wallengren J. Familial perifolliculi-
55. Levin MK, Ng E, Bae Y-SC, Brauer JA, Geronemus
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Dermatol. 1990;23(4 Pt 1):742–3. Q-switched ruby, and Q-switched Nd:YAG nano-
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Arias-Santiago S, et al. Epidemiology, clinical pre- Lasers Surg Med. 2016;48(2):181–7. https://doi.
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58. Ishiy P, Silva L, Penha M, Handel A, Miot H. Skin Zancanaro P, Vashi N. Sun-protective behaviors in
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228–37. 67. Grimes P. The safety and efficacy of salicylic acid
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Aging of the Skin
3
Enzo Berardesca, Norma Cameli, and Maria Mariano

Skin aging is generally classified as intrinsic smoke, (4) nutrition, (5) a number of less well
aging and photoaging based on the mechanism of studied, miscellaneous factors, as well as (6) cos-
action and the skin site [1]. Intrinsic aging is metic products [6]. Basically all these damage epi-
characterized by thinning of the epidermis and dermal living cells and metabolism by increasing
fine wrinkles caused by cellular aging [1, 2], reactive oxygen species formation (ROS) inducing
while photoaging is characterized by deep wrin- changes in cell metabolism and function.
kles, skin laxity, telangiectasias, and appearance From a clinical point of view an important
of lentigines, and is mainly caused by exposure to change is the thinning of the epidermis. Starting
UV and other environmental factors [1, 3]. At the at about age 30, the epidermis decreases in thick-
cellular level skin aging has been attributed to the ness at about 6.4% per decade [7]. Changes in
loss of mature collagen and increased matrix epidermal thickness are most pronounced in
metalloproteinase (MMP) expression [1–3]. exposed areas, such as the face, neck, upper part
MMP-1 is known as an initiator collagenase of the chest and the extensor surface of the hands
responsible for collagen fragmentation in skin and forearms [8] due FontCreator Pro Serial Key the accumulation of
aging process, and MMP-2 and -9 are known to intrinsic aging and extrinsic aging. Flattening of
be responsible for further degradation of collagen the dermal–epidermal junction due to a retraction
[1, 3]. Impaired TGF-β signaling caused reduc- of the rete pegs is also a feature of aged skin [7].
tion of collagen synthesis is another reason for The skin becomes less resistant to shearing forces
collagen loss in aged skin [2, 4, 5]. and more vulnerable to insult [9]. Changes in
More recently, other environmental factors microcirculation and blood supply can be respon-
have been recognized being involved in the aging sible decreased basal cell proliferation and altera-
process known as the ‘exposome’ concept; Avast Antivirus 2018 - Free Activators is tions in transcutaneous penetration [7, 10] With
generally agreed that both external and internal aging, epidermal turnover diminishes resulting in
factors as well as the response of the human body a smaller number of cell layers [11].
to these factors all add up to define the exposome.
Specifically, these can be conducted to: (1) sun
radiations: ultraviolet radiation, visible light and 3.1  hanges in Stratum
C
infrared radiation, (2) air pollution, (3) tobacco Corneum with Age

The water content movavi pdf editor review - Crack Key For U the SC decreases progres-


E. Berardesca (*) · N. Cameli · M. Mariano sively with age and eventually falls below the
San Gallicano Dermatological Institute, Rome, Italy level necessary for effective desquamation. This
e-mail: berardesca@berardesca.it

© Springer International Publishing AG, part of Springer Nature 2018 25


E. Tur, H. I. Maibach (eds.), Gender and Dermatology,
https://doi.org/10.1007/978-3-319-72156-9_3
26 E. Berardesca et al.

causes corneocytes to pile up and adhere to the time of the stratum corneum associated with
skin surface, which accounts for the roughness, increasing age [18]. The lengthening of the turn-
scaliness and flaking that accompanies xerosis in over implies a reduction in the desquamation
aged skin. The integrity of the SC barrier is rate but this is not as large as thought. The reason
dependent on an orderly arrangement of critical for this is the increase of corneocyte size during
lipids [7]. The total lipid content of the aged skin ageing. Thus there are fewer corneocytes in an
decreases dramatically, and this alteration in the old individual’s stratum corneum compared to a
lipid barrier results in dryer skin [12]. Age-related young one per volume unit. Studies measuring
changes in the amino acid composition reduce the release of corneocytes from the skin showed
the amount of cutaneous NMF, thereby decreas- also that there is a decrease of corneocyte loss at
ing the skin’s water-binding capacity [13]. least measured under these experimental condi-
There have been few attempts to measure the tions [19].
rate of corneocyte loss and desquamation in rela- The evolution of corneocyte size during the
tion with the ageing process. This is odd because ageing process has been studied by several
desquamation is a very important process. authors; there is a consensus that the size pro-
Corneocyte size and renewal (or turnover) gressively increases with age, even though there
depends not only by the rate of input into the are body site variations and seasonal variations
system (epidermopoiesis) but also on the rate at (changes due to hormonal status will be discussed
which cells are lost (desquamation). The epider- later in this document). The more investigated
mis shows a linear decrease in thickness with sites are the arm and the forearm and data shows
age, both in absolute terms and in cell number. a progressive increase of corneocyte size from
The reduction in epidermal population size sug- birth to age [20–23].
gests that there may be also a decrease in the rate Some differences have been reported between
on production of epidermal cells, and the appar- sunexposed and non sunexposed areas [24] where
ent lengthening of the stratum corneum renewal in general UV irradiation increases epidermal
time seems to confirm it. In addition, there is turnover leading to smaller corneocytes com-
some evidence that the rate of reepithelization of pared to a similar photoprotected site. Indeed,
wounds decreases with age. Using tritiated thy- seasonal variations in corneocyte size have been
midine and an autoradiographic labelling method reported with smaller corneocytes in summer as a
Kligman [14] reported a reduced value for an consequence of prolonged solar irradiation [25].
elderly cohort compared to a younger group; in a In a study on professional cyclists it was found
study comparing the effects of ageing between that the microsoft office free download for windows 10 - Crack Key For U of corneocytes from the area of the
sun exposed and non exposed sites this has not arm protected by the shirt was “normal”, while in
been detected [15]. In a more sensitive but com- the adjacent exposed area the area of the cells
plicated assay using the FACS fluorescent assay was significantly smaller [26].
it was demonstrated an age related decrease in In conclusion there is a correlation and an
the DNA synthesis and so in a longer cell cycle inverse relationship between stratum corneum
through the stratum corneum [16]. Stratum cor- turnover and dimensions of corneocytes.
neum cell turnover and replacement time have
been evaluated using also the dansyl chloride
staining technique. Dansyl chloride is a fluores- 3.2  hanges in the Dermis
C
cent dye which penetrates the full thickness of with Age
the stratum corneum and, when applied topically
to the skin in vivo, becomes florescent under At the dermal level, all three major extracellular
Wood’s light [17]. The time the fluorescente components of the dermis (collagen, elastin, and
takes to disappear corresponds to the turnover hyaluronic acid) are depleted in older skin.
cycle of the stratum corneum; these studies have Collagen content decreases at about 2% per year
shown a progressive increase in the turnover [27], due to both a decrease in collagen synthesis
3  Aging of the Skin 27

[28] and an increase in the degradation of colla- with premenopausal women [37]. Women with a
gen [29]. The relative proportions of collagen premature menopause have accelerated degener-
types are also disrupted in aged skin. The propor- ative changes in dermal elastic fibers [33]. In
tion of Type I collagen to Type III collagen in addition, decreased estrogens after menopause

Источник: https://www.scribd.com/document/454978907/Gender-and-Dermatology-by-Ethel-Tur-Howard-I-Maibach-eds-z-lib-org-pdf

My Medicine Notes

It is recommended that all children and adolescents with a new diagnosis of hypertension undergo renal ultrasound and laboratory evaluation for renal pathology (strength of recommendation [SOR]: C, consensus-based guidelines). 

Specific diagnostic tests are recommended for newly diagnosed patients who have suspicious clinical findings suggestive of a secondary cause of hypertension based on the initial history (excess daytime sleepiness, palpitations, tremor, sweating); physical examination (abdominal bruit, thyromegaly, malar rash); or laboratory analysis (elevated serum creatinine, low thyroid-stimulating hormone) (SOR: C, consensus-based guidelines). 

Patients with undifferentiated resistant hypertension should receive further directed evaluation for secondary causes (SOR: C, consensus-based guidelines).


Children:

Secondary hypertension is more prevalent in younger children and in children and adolescents with stage 2 hypertension (blood pressure [BP] >99th percentile for age and height plus 5 mm Hg).1 Renoparenchymal and renovascular disease account for most cases of secondary hypertension in these children.

70% to 85% of children <12 years and 10% to 15% of adolescents 12 to 18 years with hypertension have an underlying cause, most commonly renoparenchymal and renovascular disease.

Such evaluation should include a renal ultrasound and laboratory testing (creatinine, urinalysis, and urine culture) to look for structural or functional anomalies.

Adults:

Secondary hypertension reportedly occurs in 5% to 10% of hypertensive patients.

Patients at highest risk for secondary hypertension have no family history of hypertension; abrupt onset, symptomatic, or crisis hypertension; stage 2 hypertension; sudden loss of hypertensive control; and drug-resistant hypertension.

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recommends that patients with the following characteristics undergo further directed evaluation for a secondary cause:8

  • younger than 30 years with no family history of hypertension
  • older than 55 years with new hypertension
  • abdominal bruit with diastolic component
  • sudden worsening of BP control
  • recurrent flash pulmonary edema
  • renal failure with abnormal urinary sediment or proteinuria
  • acute renal failure after administration of an ACE inhibitor or ARB.

Patients with resistant hypertension (BP>140/90 mm Hg despite taking optimal doses of 3 antihypertensive medications, one of which is a diuretic) should receive particular scrutiny for an identifiable secondary cause.

References:

  • J Fam Pract. 2014 January;63(1):41-42,54.
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Vit Registry Fix Pro 12.6.6 Free Download with Crack

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3 Replies to “Vit Registry Fix Pro 12.6.6 Free Download with Crack”

  1. isnt that how someone begins tho? you called everyone who's still learning a noob everytime? man

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